In that work, silencing of CYP3A4 blocked the cell cycle at the G2–M checkpoint and induced apoptosis of MCF7 cells by inhibiting STAT3 (Tyr-705) phosphorylation, thereby inhibiting the growth and survival of the tumor cells; a knockdown of CYP3A5 suppressed the proliferation of cell lines MCF7, T47D, and MDA-MB-231 to various degrees [313]. Here, CYP3A4 is linked to neoplasm.