In the present study, podocyte‐specific RIPK3‐KO mice and STZ‐induced DKD mice, combined with HFD feeding and UNI, were used to exacerbate glomerular sclerosis and podocyte injury.[8] The results showed that podocyte‐specific RIPK3 KO significantly reduced glomerular mesangial matrix proliferation, foot process fusion, and podocyte loss, ultimately leading to reduced proteinuria, confirming the role of RIPK3 in podocyte injury of DKD. This evidence concerns the gene RIPK3 and diabetic kidney disease.