Attributing an observed outcome to its root cause is a central task in domains ranging from medical diagnosis to engineering fault diagnosis. Existing approaches either equate the root cause with a root node of the causal graph, as in causal-discovery-based root cause analysis, or target causes more broadly and thereby favour proximate ones, as with the probability of causation and posterior causal effects. We argue that this issue stems from the absence of a formal definition of a root cause, which has led to methods designed for other purposes being applied to root cause attribution by default. We address this by giving a formal, individual-level definition of a root cause within the potential outcomes framework, based on the notion of an individual cause and a counterfactual root condition motivated by mediation analysis. Building on this definition, we propose the probability of root cause (PRC), which quantifies how probable it is that a candidate variable set is the root cause of a given outcome, conditional on observed evidence. Under standard assumptions, we establish the identifiability of the PRC and derive an explicit identification formula. Two numerical examples illust
Separate modelling of cause specific mortality rates and their projections can yield inconsistent forecasts when the sum of deaths by cause does not match the total observed in a population. We develop a hierarchical probabilistic framework for cause specific mortality counts in which both the total number of deaths and the occurrence of deaths across causes are treated as random. Conditional on the total number of deaths, cause specific counts follow a multinomial distribution, whereas the total count is modelled using a Poisson distribution, and the vector of cause of death probabilities is assigned a Dirichlet distribution. The variation in cause specific mortality rates by age and calendar year is captured in both the Poisson and Dirichlet models, allowing interpretable demographic patterns while preserving coherence by construction. This model construction naturally preserves the coherence between the sum of deaths by cause and the total mortality. The method is exhibited through the analysis of cause specific mortality rates in the United States and France, sourced from the Human Mortality Database from 1979 to 2023, separately by sex and across ages, with deaths grouped into
Understanding and forecasting mortality by cause is an essential branch of actuarial science, with wide-ranging implications for decision-makers in public policy and industry. To accurately capture trends in cause-specific mortality, it is critical to consider dependencies between causes of death and produce forecasts by age and cause coherent with aggregate mortality forecasts. One way to achieve these aims is to model cause-specific deaths using compositional data analysis (CODA), treating the density of deaths by age and cause as a set of dependent, non-negative values that sum to one. A major drawback of standard CODA methods is the challenge of zero values, which frequently occur in cause-of-death mortality modelling. Thus, we propose using a compositional power transformation, the $α$-transformation, to model cause-specific life-table death counts. The $α$-transformation offers a statistically rigorous approach to handling zero value subgroups in CODA compared to \emph{ad-hoc} techniques: adding an arbitrarily small amount. We illustrate the $α$-transformation on England and Wales, and US death counts by cause from the Human Cause-of-Death database, for cardiovascular-related
We study distribution-free root cause analysis in multi-stream data, where an evolving underlying system is observed through multiple data streams that may each undergo distributional changes at unknown timepoints. In such settings, the stream exhibiting the earliest change provides a natural starting point for investigating the underlying cause, which we refer to as the root-cause index. Leveraging conformal $p$-values, we propose a novel framework, Conformal Root Cause Analysis (CROC), which constructs finite-sample valid confidence sets for the root-cause index under minimal assumptions: the data streams are independent, and within each stream the pre- and post-change observations are sampled exchangeably from arbitrary and unknown distributions. We further establish a universality property, showing that any distribution-free method for root cause localization can be represented within the CROC framework. In addition, under mild regularity conditions and principled score design, our method yields asymptotically sharp confidence sets that efficiently isolate the root cause. We further extend CROC to efficiently handle cross-stream dependence when present. Extensive simulations de
Recently, Batusov and Soutchanski proposed a notion of actual achievement cause in the situation calculus, amongst others, they can determine the cause of quantified effects in a given action history. While intuitively appealing, this notion of cause is not defined in a counterfactual perspective. In this paper, we propose a notion of cause based on counterfactual analysis. In the context of action history, we show that our notion of cause generalizes naturally to a notion of achievement cause. We analyze the relationship between our notion of the achievement cause and the achievement cause by Batusov and Soutchanski. Finally, we relate our account of cause to Halpern and Pearl's account of actual causality. Particularly, we note some nuances in applying a counterfactual viewpoint to disjunctive goals, a common thorn in definitions of actual causes.
Not much has been written about the role of triggers in the literature on causal reasoning, causal modeling, or philosophy. In this paper, we focus on describing triggers and causes in the metaphysical sense and on characterizations that differentiate them from each other. We carry out a philosophical analysis of these differences. From this, we formulate a definition that clearly differentiates triggers from causes and can be used for causal reasoning in natural sciences. We propose a mathematical model and the Cause-Trigger algorithm, which, based on given data to observable processes, is able to determine whether a process is a cause or a trigger of an effect. The possibility to distinguish triggers from causes directly from data makes the algorithm a useful tool in natural sciences using observational data, but also for real-world scenarios. For example, knowing the processes that trigger causes of a tropical storm could give politicians time to develop actions such as evacuation the population. Similarly, knowing the triggers of processes that cause global warming could help politicians focus on effective actions. We demonstrate our algorithm on the climatological data of two
The sufficient cause framework has been used for decades to improve our understanding of both basic and more complex causal concepts in epidemiology, such as mediation and interaction. Here, we make use of this framework to provide a description of truncation by death, in which the outcome of interest is undefined for individuals who die before the time of assessment at the end of follow-up. We explain the non-causal nature of the crude estimand that compares outcomes by treatment levels conditional on observed survival by showing that it corresponds to a comparison of distinct risk status types, which are defined based on the susceptibility to sufficient causes. Further, expressions for the crude estimand and for the survivor average causal effect, a causal estimand defined under the principal stratification approach, are provided in terms of population-level joint frequencies of the background factors of sufficient causes. Finally, we also describe conditions, based on background factors of sufficient causes, under which the survivor average causal effect is null. Our description of this problem, which studies truncation by death from a new perspective, might encourage further an
We propose a novel causal principle that is a genuinely multipartite extension of Reichenbach's common cause principle, namely, the coordination principle: parties in a network can achieve perfect randomized coordination--in particular, agree on a uniformly random output--only if they all share a common cause. We show that this principle does not follow from the standard no-signaling and independence principles by providing an explicit theory satisfying all these principles while violating the coordination principle. Strikingly, we prove that the coordination principle holds, however, in quantum theory for four parties, and derive noise-tolerant Bell-like inequalities that certify a common cause. We then extend these results to a genuinely quantum coordination task, showing that the four-partite GHZ state requires a quantum common cause which can also be certified by experimentally accessible Bell-like inequalities. A companion paper generalizes these results for N parties, proving that the coordination principle is satisfied in general for quantum theory.
Failures in complex systems demand rapid Root Cause Analysis (RCA) to prevent cascading damage. Existing RCA methods that operate without dependency graph typically assume that the root cause having the highest anomaly score. This assumption fails when faults propagate, as a small delay at the root cause can accumulate into a much larger anomaly downstream. In this paper, we propose PRISM, a simple and efficient framework for RCA when the dependency graph is absent. We formulate a class of component-based systems under which PRISM performs RCA with theoretical guarantees. On 735 failures across 9 real-world datasets, PRISM achieves 68% Top-1 accuracy, a 258% improvement over the best baseline, while requiring only 8ms per diagnosis.
In the aftermath of the COVID-19 pandemic, empirical data have revealed that large-scale health crises not only cause immediate disruptions in mortality dynamics but also have persistent effects that may last for several years. Existing mortality models largely assume that mortality shocks are transitory and overlook how their effects can be long-lasting and heterogeneous across age groups and causes of death. In response to this limitation, we propose a novel stochastic mortality model that captures age- and cause-specific long-lasting effects of mortality jumps through a gamma-density-like decay function, estimated via a customized conditional maximum likelihood algorithm. Applying the model to recent U.S. mortality data, we reveal divergent persistence patterns across demographic groups and provide key insights into the tail risk profiles of life insurance and annuity products. Our scenario-based analyses further show that neglecting persistent shock effects can lead to suboptimal hedging, while the proposed model enables what-if testing to analyze such effects under potential future health crises.
This work is motivated by the following problem: Can we identify the disease-causing gene in a patient affected by a monogenic disorder? This problem is an instance of root cause discovery. In particular, we aim to identify the intervened variable in one interventional sample using a set of observational samples as reference. We consider a linear structural equation model where the causal ordering is unknown. We begin by examining a simple method that uses squared z-scores and characterize the conditions under which this method succeeds and fails, showing that it generally cannot identify the root cause. We then prove, without additional assumptions, that the root cause is identifiable even if the causal ordering is not. Two key ingredients of this identifiability result are the use of permutations and the Cholesky decomposition, which allow us to exploit an invariant property across different permutations to discover the root cause. Furthermore, we characterize permutations that yield the correct root cause and, based on this, propose a valid method for root cause discovery. We also adapt this approach to high-dimensional settings. Finally, we evaluate the performance of our metho
Diagnosing the root cause of an anomaly in a complex interconnected system is a pressing problem in today's cloud services and industrial operations. We propose In-Distribution Interventions (IDI), a novel algorithm that predicts root cause as nodes that meet two criteria: 1) **Anomaly:** root cause nodes should take on anomalous values; 2) **Fix:** had the root cause nodes assumed usual values, the target node would not have been anomalous. Prior methods of assessing the fix condition rely on counterfactuals inferred from a Structural Causal Model (SCM) trained on historical data. But since anomalies are rare and fall outside the training distribution, the fitted SCMs yield unreliable counterfactual estimates. IDI overcomes this by relying on interventional estimates obtained by solely probing the fitted SCM at in-distribution inputs. We present a theoretical analysis comparing and bounding the errors in assessing the fix condition using interventional and counterfactual estimates. We then conduct experiments by systematically varying the SCM's complexity to demonstrate the cases where IDI's interventional approach outperforms the counterfactual approach and vice versa. Experiment
We study the propagation of outliers in cyclic causal graphs with linear structural equations, tracing them back to one or several "root cause" nodes. We show that it is possible to identify a short list of potential root causes provided that the perturbation is sufficiently strong and propagates according to the same structural equations as in the normal mode. This shortlist consists of the true root causes together with those of its parents lying on a cycle with the root cause. Notably, our method does not require prior knowledge of the causal graph.
The sufficient-component cause framework assumes the existence of sets of sufficient causes that bring about an event. For a binary outcome and an arbitrary number of binary causes any set of potential outcomes can be replicated by positing a set of sufficient causes; typically this representation is not unique. A sufficient cause interaction is said to be present if within all representations there exists a sufficient cause in which two or more particular causes are all present. A singular interaction is said to be present if for some subset of individuals there is a unique minimal sufficient cause. Empirical and counterfactual conditions are given for sufficient cause interactions and singular interactions between an arbitrary number of causes. Conditions are given for cases in which none, some or all of a given set of causes affect the outcome monotonically. The relations between these results, interactions in linear statistical models and Pearl's probability of causation are discussed.
The existing emotion-cause pair extraction (ECPE) task, unfortunately, ignores extracting the emotion type and cause type, while these fine-grained meta-information can be practically useful in real-world applications, i.e., chat robots and empathic dialog generation. Also the current ECPE is limited to the scenario of single text piece, while neglecting the studies at dialog level that should have more realistic values. In this paper, we extend the ECPE task with a broader definition and scenario, presenting a new task, Emotion-Cause Quadruple Extraction in Dialogs (ECQED), which requires detecting emotion-cause utterance pairs and emotion and cause types. We present an ECQED model based on a structural and semantic heterogeneous graph as well as a parallel grid tagging scheme, which advances in effectively incorporating the dialog context structure, meanwhile solving the challenging overlapped quadruple issue. Via experiments we show that introducing the fine-grained emotion and cause features evidently helps better dialog generation. Also our proposed ECQED system shows exceptional superiority over baselines on both the emotion-cause quadruple or pair extraction tasks, meanwhile
Identifying upstream processes responsible for wafer defects is challenging due to the combinatorial nature of process flows and the inherent variability in processing routes, which arises from factors such as rework operations and random process waiting times. This paper presents a novel framework for wafer defect root cause analysis, called Partial Trajectory Regression (PTR). The proposed framework is carefully designed to address the limitations of conventional vector-based regression models, particularly in handling variable-length processing routes that span a large number of heterogeneous physical processes. To compute the attribution score of each process given a detected high defect density on a specific wafer, we propose a new algorithm that compares two counterfactual outcomes derived from partial process trajectories. This is enabled by new representation learning methods, proc2vec and route2vec. We demonstrate the effectiveness of the proposed framework using real wafer history data from the NY CREATES fab in Albany.
The common cause principle for two random variables $A$ and $B$ is examined in the case of causal insufficiency, when their common cause $C$ is known to exist, but only the joint probability of $A$ and $B$ is observed. As a result, $C$ cannot be uniquely identified (the latent confounder problem). We show that the generalized maximum likelihood method can be applied to this situation and allows identification of $C$ that is consistent with the common cause principle. It closely relates to the maximum entropy principle. Investigation of the two binary symmetric variables reveals a non-analytic behavior of conditional probabilities reminiscent of a second-order phase transition. This occurs during the transition from correlation to anti-correlation in the observed probability distribution. The relation between the generalized likelihood approach and alternative methods, such as predictive likelihood and the minimum common cause entropy, is discussed. The consideration of the common cause for three observed variables (and one hidden cause) uncovers causal structures that defy representation through directed acyclic graphs with the Markov condition.
In this paper we propose a dynamic model of Common Cause Failures (CCF) that allows to generate common cause events in time. The proposed model is a generalization of Binomial Failure Rate Model (Atwood model) that can generate staggered failures of multiple components due to a common cause. We implement the model using statechart formalism, a similar implementation can be adopted in other modeling languages like Petri Nets or Hybrid Stochastic Automata. The presented model was integrated in a Dynamic PRA study.
The task of Emotion-Cause Pair Extraction (ECPE) aims to extract all potential emotion-cause pairs of a document without any annotation of emotion or cause clauses. Previous approaches on ECPE have tried to improve conventional two-step processing schemes by using complex architectures for modeling emotion-cause interaction. In this paper, we cast the ECPE task to the question answering (QA) problem and propose simple yet effective BERT-based solutions to tackle it. Given a document, our Guided-QA model first predicts the best emotion clause using a fixed question. Then the predicted emotion is used as a question to predict the most potential cause for the emotion. We evaluate our model on a standard ECPE corpus. The experimental results show that despite its simplicity, our Guided-QA achieves promising results and is easy to reproduce. The code of Guided-QA is also provided.
Reichenbach defined a common cause which explains a correlation between two events if either one does not cause the other. Its intuitive idea is that the statistical ensemble can be divided into two disjoint parts so that the correlation disappears in both of the resulting subensembles if there is no causal connection between these correlated events. These subensembles can be regarded as common causes. Hofer-Szabó and Rédei (2004) generalized a Reichenbachian common cause, and called it a Reichenbachian common cause system. In the case of Reichenbachian common cause systems the statistical ensemble is divided more than two, while it is divided into two parts in the case of Reichenbachian common causes. The number of these subensembles is called the size of this system. In the present paper, we examine Reichenbachian common cause systems in general probability theories which include classical probability theories and quantum probability theories. It is shown that there is no Reichenbachian common cause system for any correlation between two events which are not logical independent, and that a general probability theory which is represented by an atomless orthomodular lattice with a