OXPHOS damage is ever known to promote HIF-1α stabilization in normoxia and hypoxia, however, a series of studies noted that OXPHOS damage accompanied with mitochondrial complex I (CI) dysfunction may reduce HIF-1α activity, and glycolysis reduced by 5′ AMP-activated protein kinase (AMPK) is negatively associated with HIF-1α activity due to ATP supply and reactive oxygen species (ROS) production which promotes tumor progression [58–61]. Here, HIF1A is linked to neoplasm.