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ARID1A, a subunit of the SWI\/SNF complex, is mutated in approximately 20% of all bladder tumors; however, the consequences of this remain poorly understood. Finding truncations to be the most common mutation, we generated loss\u2010 and gain\u2010of\u2010function models to conduct RNA\u2010Seq, interactome analyses, Omni\u2010ATAC\u2010Seq, and functional studies to characterize ARID1A\u2010affected pathways potentially suitable for the treatment of ARID1A\u2010deficient bladder cancers. We observed decreased cell proliferation and deregulation of stress\u2010regulated pathways, including DNA repair, in ARID1A\u2010deficient cells. Furthermore, ARID1A was linked to alternative splicing and translational regulation on RNA and interactome levels. ARID1A deficiency drastically reduced the accessibility of chromatin, especially around introns and distal enhancers, in a functional enrichment analysis. 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