Although the administration of exogenous leptin reportedly accelerated the development of NASH in a NASH rodent model, in which the hepatic Leprb expression remained detectable42, clinical findings have revealed that treatment with exogenous leptin attenuated hepatosteatosis and hepatocellular ballooning injuries seen in NASH patients with leptin-deficient lipodystrophy. Here, LEP is linked to metabolic dysfunction-associated steatohepatitis.