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. Here, HNF4A is linked to Familial prostate cancer.