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Summary Statistical hypotheses are translations of scientific hypotheses into statements about one or more distributions, often concerning their centre. Tests that assess statistical hypotheses of centre implicitly assume a specific centre, e.g., the mean or median. Yet, scientific hypotheses do not always specify a particular centre. This ambiguity leaves the possibility for a gap between scientific theory and statistical practice that can lead to rejection of a true null. In the face of replicability crises in many scientific disciplines, significant results of this kind are concerning. Rather than testing a single centre, this paper proposes testing a family of plausible centres, such as that induced by the Huber loss function. Each centre in the family generates a testing problem, and the resulting family of hypotheses constitutes a familial hypothesis. A Bayesian nonparametric procedure is devised to test familial hypotheses, enabled by a novel pathwise optimization routine to fit the Huber family. The favourable properties of the new test are demonstrated theoretically and experimentally. Two examples from psychology serve as real-world case studies. 

Abstract Investigating the causal relationship between exposure and time-to-event outcome is an important topic in biomedical research. Previous literature has discussed the potential issues of using hazard ratio (HR) as the marginal causal effect measure due to noncollapsibility. In this article, we advocate using restricted mean survival time (RMST) difference as a marginal causal effect measure, which is collapsible and has a simple interpretation as the difference of area under survival curves over a certain time horizon. To address both measured and unmeasured confounding, a matched design with sensitivity analysis is proposed. Matching is used to pair similar treated and untreated subjects together, which is generally more robust than outcome modeling due to potential misspecifications. Our propensity score matched RMST difference estimator is shown to be asymptotically unbiased, and the corresponding variance estimator is calculated by accounting for the correlation due to matching. Simulation studies also demonstrate that our method has adequate empirical performance and outperforms several competing methods used in practice. To assess the impact of unmeasured confounding, we develop a sensitivity analysis strategy by adapting the E -value approach to matched data. We apply the proposed method to the Atherosclerosis Risk in Communities Study (ARIC) to examine the causal effect of smoking on stroke-free survival.