VHL and neoplasm: On the other hand, in hypoxia condition HIFα is not prolyl hydroxylated and may escape pVHL recognition, resulting in accumulation of HIFα and formation of a complex with HIF1β, goes into the nucleus and activates a transcriptional program to cope with the short-term, long-term effects of oxygen deprivation, several signaling pathways as well as angiogenesis factor for leading cell proliferation or tumor [14,15].