Selective inhibition of CYP2C9 decreased tumor cell proliferation and led to a G0/G1 phase cell-cycle arrest in vitro, which was abolished by the addition of 11,12-EET.388,390 Moreover, CYP3A4 is a highly active AA epoxygenase and synthesized AA epoxygenase products 8,9-, 11,12-, and 14,15-EET in the breast cancer lines.391 CYP3A4 silencing blocked the cell cycle at the G2/M checkpoint and induced apoptosis in the MCF7 line via inhibiting Stat3 (Tyr-705) phosphorylation, thereby inhibiting anchorage-dependent growth and survival. The gene discussed is CYP3A4; the disease is neoplasm.