Interestingly, a feed forward loop seems to exist in PCa between STAT3, oncogenic signaling and HIF-1α mediated angiogenesis; as STAT3 can directly inhibit p53 and p53 acts as an inhibitor of HIF-1α, it may be that in PCa where STAT3 is constitutively active there is further downstream activation of HIF-1α and VEGF. The gene discussed is HIF1A; the disease is posterior cortical atrophy.