In a unilateral ureteral obstruction induced renal fibrosis model, RIPK3 promotes fibrotic progression via AKT‐dependent activation of ATP‐citrate lyase, independent of MLKL‐mediated necroptosis.[21] Furthermore, in cardiac ischemia‐reperfusion injury models, RIPK3 exacerbates mitochondrial‐mediated apoptosis by suppressing FUNDC1‐dependent mitophagy.[22] Although some studies have reported HG‐induced RIPK3/pMLKL activation and necroptosis in podocytes in vitro,[13, 17] such pronounced morphological abnormalities of podocyte necrosis are not characteristic pathological features of DKD. This evidence concerns the gene MLKL and diabetic kidney disease.