Some studies have demonstrated that HIFs are participants in the regulation of pro-fibrotic genes and the promotion of renal fibrosis via TGF-β, NF-κB, and the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway or via G2/M cell cycle arrest pathway through p53 upregulation [101,102]. The gene discussed is AKT1; the disease is renal fibrosis.