Furthermore, another important finding in this study was that lncARSR activated the IRS2/AKT pathway to elevate lipid accumulation in vivo and in vitro, accompanied by increased expression of Fasn, Scd1 and GPA, and accelerate NAFLD progression through inhibition of YAP1 phosphorylation. This evidence concerns the gene LNCARSR and metabolic dysfunction-associated steatotic liver disease.