The consequent generation of inflammatory mediators like IFNγ, IL-2, IL10, GM-CSF, TGF-β, CXCL1, IL-6, MIP-2, and MCP-1 by tubular and endothelial cells are thought to play an important role in AKI pathophysiology [37]–[41]. The gene discussed is TGFB1; the disease is acute kidney injury.