MG53 (also named TRIM72) was also proved to inhibit the activation of NF-κB and attenuated renal fibrosis by binding to p65 and blocking its nucleus translocation.236 The activation of NF-κB decreased the level of TYRO3 which was a podocyte protective factor in glomerular disease.237 Protein S inhibited the TNF-α induced NF-κB activation in a TYRO3 receptor-dependent way.238. The gene discussed is NFKB1; the disease is glomerular disorder.