Tubule‐specific Lonp1 overexpression mitigated mitochondrial dysfunction and markedly increased tubular injury and renal fibrosis in two mouse models of CKD (one involving unilateral ureteral obstruction [UUO] and one involving 5/6 nephrectomy [5/6Nx]), but these outcomes were aggravated by tubule‐specific Lonp1 abrogation. This evidence concerns the gene LONP1 and chronic kidney disease.