Renal mitochondrial dysfunction often exhibits as an induction of pro‐inflammatory cytokines resulting in inflammatory damage and accumulation of lipid deposit leading to renal lipotoxicity.5 Peroxisome proliferator‐activated receptor (PPAR) γ coactivator 1α (PGC1α), 5’ AMP‐activated protein kinase (AMPK) and sirtuin (SIRT) pathways are potential molecular signalling mediating the pathophysiological changes in obesity‐induced renal diseases.6, 7, 8 However, it is still need to further explore more valuable therapeutic targets to combat renal lipotoxicity and dysfunction. The gene discussed is PPARGC1A; the disease is obesity due to melanocortin 4 receptor deficiency.