In the current study, wild-type (WT) and BAP31 conditional knockout (KO) mice were treated with Tm to induce ER stress, which increased hepatic lipid accumulation, markers of ER stress, liver steatosis, and the underlying mechanisms will be evaluated, to explore whether BAP31 plays a role in lipid accumulation, and if it prevents the development of fatty liver disease via modulating ER stress status. This evidence concerns the gene BCAP31 and fatty liver disease.