Subsequent work by Bitler et al has shown that ARID1A‐mutated ovarian cancers are selectively dependent on HDAC6 activity, due to HDAC6 upregulation in ARID1A mutant cells that mechanistically inactivates the apoptosis‐promoting function of TP53 due to deacetylation of histone lysine 120 [22]. This evidence concerns the gene ARID1A and ovarian cancer.