The relationship between BNIP3 and AR expressions would be explained through the mechanism of autocrine loop of tyrosine kinase receptor/phosphatidylinositol 3′-kinase/protein kinase B. In a AR positive prostate cancer cell study, androgen had activated this tyrosine kinase receptor/phosphatidylinositol 3′-kinase/protein kinase B which increases HIF-1α and HIF-α regulated gene expression [30]. The gene discussed is HIF1A; the disease is Familial prostate cancer.