It follows, then, that PBRM1, ARID2, and BRD7 genomic alterations that increase chromatin accessibility to IFN‐responsive genes may sensitize cancer cells to therapeutics that rely on T cell‐mediated cytotoxicity for their mechanism of action, including ICI, T cell engagers, and chimeric antigen receptor T cells [54]. The gene discussed is PBRM1; the disease is cancer.