Non-alcoholic fatty liver disease (NAFLD) is associated with lipid accumulation in hepatocyte. NAFLD advances into NASH. It has been implicated that STARD10 gene expression is epigenetically regulated by methylation in the liver of NAFLD patients. We found STARD10 is highly expressed in the liver and involved in bile acid metabolism by regulating PPARĪ± activity. Our study also indicated that STARD10 is involved in lipid droplet (LD) formation.The purpose of this study was to elucidate the role of STARD10 in the development of NASH. We compared the lipid accumulation in the liver of NASH model mice that were induced by choline-deficient L-amino acid-defined diet (CDAA) between WT and Stard10-/- mice. The total LD area of Stard10-/- mice was significantly smaller than that of WT mice. Gene expression levels of proinflammatory cytokines and fibrosis marker genes were significantly lower in the liver of Stard10-/- mice compared with WT mice. Since cytokines released from Kupffer cells progress NASH, we confirmed that there is no Stard10 expression in Kupffer cells. Lipopolysaccharide induced the gene expression of proinflammatory cytokines in the Kupffer cells isolated from WT mice and Stard10-/- mice in the same manner. In conclusion, STARD10 is involved in the development of NASH by regulating LD formation in hepatocyte.