Jana et al. now show a similar conflict in AT-rich interactive domain-containing protein 1 A (ARID1A), a SWI/SNF nucleosome remodeler mutated in ~25% urothelial malignancies.1 ARID1A is thought to be a tumor suppressor because its deletion upregulates transcription of oncogenic transcripts and promotes double stranded DNA (dsDNA) break repair, which results in tumor progression. Here, ARID1A is linked to neoplasm.