In the liver, BPA increased de novo lipogenesis by inhibiting miR192, consequently leading to the development of nonalcoholic fatty liver disease (NAFLD).[2a] By targeting Pdx‐1, miR338 controlled the BPA‐induced pancreatic insulin secretory of epigenetic information transmission, some miRNAs have been reported to exhibit consistent changes in the liver of father‐offspring pairs of animals. Here, PDX1 is linked to metabolic dysfunction-associated steatotic liver disease.