For instances, NAT10 directly acetylates MORC2 to sensitize DNA-damaging, which potentiates the efficacy of chemotherapy and radiotherapy in breast cancer [8]; NAT10 is reported as a cellular stress sensor which acetylates p53 and counteracts Mdm2 action, thus eliciting p53 activation under DNA damage-related stress [9]; NAT10 interacts with Che-1 in the anabolism-catabolism transition in response to energy stress [10]. This evidence concerns the gene TP53 and breast cancer.