The knockdown of HNF4α could significantly promote both the in vitro and in vivo malignant growth capacities (including cell proliferation, resistance to drug-induced senescence, resistance to androgen-deprivation and paclitaxel, colony formation, and in vivo tumorigenicity) of prostate cancer cells; and conversely, its overexpression could induce cellular senescence and cell-cycle arrest in prostate cancer cells. The gene discussed is HNF4A; the disease is prostate carcinoma.