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Readers of Hannah Arendt’s now classic formulation of the statelessness problem in her 1951 book The Origins of Totalitarianism abound at a moment when the number of stateless peoples worldwide continues to rise exponentially. Along with statelessness, few concepts in Arendt scholarship have spawned such a volume of literature, and perhaps none have provoked as much interest outside of the field of philosophy, as ‘the right to have rights.’ Interpreting this enigmatic term exposes the heart of our beliefs about the nature of the political and has important consequences for how we practice politics on a global scale because it implicitly takes plural human beings, and not the citizen, as its subjects. Arendt’s conceptualization of this problem remains unsurpassed in its diagnosis of the political situation of statelessness, as well as its intimate description of the human cost of what she refers to as ‘world loss,’ a phenomenon that the prevailing human rights and global justice discourse does not take into account. And yet, as an alternative framework for thinking about global politics, the right to have rights resists easy interpretation, let alone practical application.
Bipolar disorder (BD) is a heritable mental illness with complex etiology. While the largest published genome-wide association study identified 64 BD risk loci, the causal SNPs and genes within these loci remain unknown. We applied a suite of statistical and functional fine-mapping methods to these loci, and prioritized 22 likely causal SNPs for BD. We mapped these SNPs to genes, and investigated their likely functional consequences by integrating variant annotations, brain cell-type epigenomic annotations, brain quantitative trait loci, and results from rare variant exome sequencing in BD. Convergent lines of evidence supported the roles of SCN2A, TRANK1, DCLK3, INSYN2B, SYNE1, THSD7A, CACNA1B, TUBBP5, PLCB3, PRDX5, KCNK4, AP001453.3, TRPT1, FKBP2, DNAJC4, RASGRP1, FURIN, FES, YWHAE, DPH1, GSDMB, MED24, THRA, EEF1A2, and KCNQ2 in BD. These represent promising candidates for functional experiments to understand biological mechanisms and therapeutic potential. Additionally, we demonstrated that fine-mapping effect sizes can improve performance and transferability of BD polygenic risk scores across ancestrally diverse populations, and present a high-throughput fine-mapping pipeline (https://github.com/mkoromina/SAFFARI).