The 148 M PNPLA3 allele was previously associated with adipocytes of smaller size, a marker of metabolic derangement, and increased leptin transcription in a small group of obese children with NAFLD [26], thus suggesting that modulation of adipose tissue endocrine activity may be implicated in the mechanism by which PNPLA3 influences NASH susceptibility. This evidence concerns the gene LEP and metabolic dysfunction-associated steatohepatitis.