TGFB1 and acute kidney injury: These M2 macrophages continually produce growth factors/cytokines, such as TGF‐β1 and epidermal growth factor (EGF), which induce activation of interstitial fibroblasts, leading to excessive ECM deposition and the progression of kidney fibrosis.[84] Therefore, regulation of the M1/M2 phenotype balance represents a critical mechanism in the treatment of AKI.