Overexpression of these 3 proteins induced MCF-7 cells to enter the S-phase even in the presence of chemotherapy drugs with attenuated checkpoint activation, strongly suggesting that aberrant AP-2γ activity may contribute to the failure of chemotherapy in breast cancer.[39] In contrast, in triple-negative MDA-MB-231 cells, overexpression of AP-2γ led to cell cycle arrest with induced CDKN1A expression,[40] highlighting the AP-2γ might exert different (even contradictory) functions in cell cycle regulation in different breast cancer subtypes. The gene discussed is CDKN1A; the disease is breast cancer.