Nevertheless, we suggest that ANT2 depletion in RPTCs under lipotoxic conditions may trigger a long-lasting protective metabolic rewiring toward glycolysis by a compensatory upregulation of ANT4 expression, allowing these cells to maintain energy production, which in turn promotes the preservation of renal function and ameliorates obesity-induced CKD. The gene discussed is SLC25A5; the disease is obesity due to melanocortin 4 receptor deficiency.