We observed a significant upregulation of ATG5 in human tubular epithelial cells (HK‐2) stimulated with uric acid (UA), aristolochic acid (AA) and transforming growth factor‐β1 (TGF‐β1), as well as in kidney tissue samples from patients with CKD and in mice models of hyperuricemic nephropathy (HN), aristolochic acid nephropathy (AAN) and unilateral renal ischemia‐reperfusion injury (uIRI), three independent models of kidney fibrosis. The gene discussed is TGFB1; the disease is Balkan nephropathy.