To elucidate the molecular mechanism by which zinc affects the HIF-1/VEGF signalling, we took advantage of an ex vivo experimental model consisting of cell populations derived from explants of prostate cancer patients [19] characterized by a “constitutively hypoxic” phenotype (e.g., stabilized HIF-1α and HIF-2α protein in normoxia, namely C27) associated with bad prognosis and a phenotype negative for HIF-1α and HIF-2α expression under aerobic condition associated with good prognosis (namely C38) [9]. The gene discussed is EPAS1; the disease is Familial prostate cancer.