For example, KDM6A appears to support stemness in solid tumors responding to therapy by: (1) activating pluripotency genes,109 (2) cooperating with H3 acetylation as mediated by E1A binding protein p300 (EP300), at least in the context of breast cancer,110 or (3) promoting a switch toward reduced proliferation coupled with a global redistribution of H3K27 marks and upregulated NOTCH signaling, as observed in GSCs.111 However, mutations in KDM6A are common in multiple cancer types, potentially suggesting a suppressive role in CSC maintenance. This evidence concerns the gene EP300 and breast carcinoma.