Immunohistochemistry revealed that renal fibrosis, evidenced by increased α-SMA+ myofibroblasts and Col-1 and FN accumulation, was associated with substantial activation of p-Smad3, downregulation of GPX4, and increased biomarkers of ferroptosis as demonstrated by upregulation of 4-HNE and TFR1 in patients with DKD and IgAN (Figure 1B, C, F). This evidence concerns the gene SMAD3 and diabetic kidney disease.