However, when the insult is severe and unresolvable, some cells fail to redifferentiate and continue to produce growth factors such as TGF-β, finally leading to renal fibrosis.119 Additionally, a recent study showed that TGF-βRII deletion in macrophages prevents tubulointerstitial fibrosis following severe ischemic renal injury by abrogating TGF-β-dependent chemoattraction of macrophages.118 Collectively, the functions of TGF-β/Smads may vary according to their activation level, disease stages, and types of AKI models, which need to be further validated. This evidence concerns the gene TGFB1 and acute kidney injury.