Specifically, TSA/SAHA (HDAC inhibitors), decitabine (DAC, DNMT1, 3a, 3b inhibitor), and JQ1 (BRD2, 3, 4 & T) stably reduced mammary stem/progenitor function in vivo, where DAC also significantly delayed tumor latency and reduced tumor incidence of p53‐driven mammary cancer. The gene discussed is DNMT1; the disease is neoplasm.