PANK1 is required for the hepatic CoA increase during the transition from glucose utilization to FAO that occurs in the fasted state.6 PANK1 is highly expressed in the liver and corresponds to the liver possessing the highest concentration of CoA.7 Deletion of PANK1 in ob/ob mice dramatically suppressed hepatic gluconeogenesis, hyperglycaemia and hyperinsulinemia without affecting insulin signalling.4 However, the role of PANK1 in metabolic reprogramming and IR induced by HFD is unclear. Here, PANK1 is linked to hyperinsulinism.