Although the I148M variant directly interferes with hepatic lipid metabolism [23-25], it has also been reported to influence adipocytes size and leptin transcription in obese children with NAFLD [26], and in mice deletion of Pnpla3 influenced gene expression in adipose tissue [25], thus suggesting that modulation of adipose tissue function might be involved in the pathogenesis of liver disease associated with the I148M polymorphism. The gene discussed is LEP; the disease is metabolic dysfunction-associated steatotic liver disease.