Importantly, although AKI is likely a multi-faceted process and varies in its pathophysiology depending upon the nature of the initiating injury (e.g., sepsis vs. polytrauma), the transition to fibrotic repair and CKD is transcriptionally preserved among different types of CKD pathophysiology and implicates the immune system, renal parenchymal hypoxia, and pro-fibrotic growth factor signaling molecules such as TGF-β (145–147). The gene discussed is TGFB1; the disease is chronic kidney disease.