As shown in Fig 1, the findings that Siah controls levels and activity of HIF-1α, which cooperates transcriptionally with FoxA2 to promote NE tumor development or formation of NED of human prostate cancers, provide a rationale for targeting the Siah/HIF/FoxA2 axis as a new therapeutic modality. The gene discussed is HIF1A; the disease is Familial prostate cancer.