This robust evidence corroborated the early evidence on the impact of the I148M PNPLA3 variant in the MASLD disease activity, where it was initially associated with liver steatosis (p = 0.03), portal inflammation (p < 0.05), lobular inflammation (p = 0.005), Mallory‐Denk bodies (p = 0.015) and fibrosis (p < 0.05), with a slight but positive significance of younger age of diagnosis (p = 0.045) [47]. Here, PNPLA3 is linked to Hepatic steatosis.