Furthermore, Snhg3 increased the expression, stability, and nuclear localization of SND1 protein by interacting with SND1, thus enhancing the expression of PPARγ via reducing H3K27me3 enrichment and boosting chromatin loose remodeling at the Pparg promoter, indicating that SND1/H3K27me3/PPARγ is partially responsible for Snhg3-induced hepatic steatosis. This evidence concerns the gene PPARG and fatty liver disease.