In contrast, in the chronic inflammatory disease NASH, HIF‐2α promotes the replacement of embryonic hepatic koilocytes by bone marrow‐derived RHMs, which are high in proinflammatory genes, by activating the PI3K/Akt/mTOR signaling pathway leading to decreased expression of lysosomal and phagocytic genes, and HIF‐2α can also activate the NF‐κB in human hepatocellular carcinoma cells (HepG2) signaling pathway to promote liver fibrosis and inflammation [44, 58]. The gene discussed is NFKB1; the disease is Hepatic fibrosis.