Importantly, in wild‐type ARID1A cells EZH2 inhibition did not display any significant impact on cell proliferation demonstrating the specificity of this effect to ARID1A mutant ovarian cancers and underscoring the critical actionability of patients' tumor genotype in clinical practice,59 and more specifically the way in which patient‐specific mutations and a mechanistic understanding of dysregulation in chromatin pathways can jointly inform rational therapeutic innovation. The gene discussed is EZH2; the disease is neoplasm.