Conversely, DNMT1 knockdown induces EMT and cancer stem‐like phenotypes in prostate cancer.[25] Down‐regulation of DNMT1 increases self‐renewal potential of hepatoma cells.[26] Our finding proves that the high mannose CD133–DNMT1 interaction maintains the slow‐cycling state and tumorigenic potential of GSC, providing a potential strategy to eliminate quiescent GSCs. The gene discussed is DNMT1; the disease is Familial prostate cancer.