Since the tumor suppressor gene VHL was identified as the key point of the Von Hippel-Lindau (VHL) disease in 19931, it has been clearly proved that hypoxia or gene mutation could lead to the inactivation of VHL and induce the loss function of VHL complex (VBC, including elongin B and C), which targeting hypoxia-inducible factors (HIFs) for ubiquitylation and proteasomal degradation2–5. Here, VHL is linked to regulation of cell cycle.