There is increasing evidence that ER stress plays an essential role in promoting the progression of NAFLD (Leamy et al., 2013; Ashraf and Sheikh, 2015; Ao et al., 2016; Xu et al., 2017), and when ER stress initiated by intracellular calcium imbalance and/or accumulation of unfolded protein, GRP78, PERK and CHOP are upregulated, initiating the unfolded protein response. This evidence concerns the gene HSPA5 and metabolic dysfunction-associated steatotic liver disease.