Surprisingly, white adipose tissue, the previously reported source of asprosin, specific knockdown of asprosin failed to alleviate hepatic steatosis and dyslipidemia in the HFCDAA diet‐induced model, suggesting that therapeutic interventions targeting asprosin for the treatment of MASLD/MASH should specifically target hepatocytes rather than adipose tissue. This evidence concerns the gene FBN1 and fatty liver disease.