In this light, given that COVID-19 seems to be associated with a hyper-ferritinaemia and in some cases, hepatic failure associated with iron overload [27], it may be relevant that V-ATPase is also key in controlling HIF1α by modulating iron levels; V-ATPase depletion/inhibition enhances HIF1α activity by depleting transferrin uptake [87]. The gene discussed is HIF1A; the disease is liver failure.