Acknowledging the unique etiological mechanisms of the initial AKI insult (359, 360), injury of proximal tubule cells in severe AKI may result in cell cycle arrest in the G2/M phase, which leads to the secretion of TGF-β and connective tissue growth factor, both of which mediate fibrosis through c-jun NH2-terminal kinase (JNK) signaling (359, 361). The gene discussed is MAPK8; the disease is acute kidney injury.