Our rationale for using an in vitro steatosis model is twofold: firstly, as a precursor of NAFLD, hepatic steatosis plays a vital role in the pathological process of NAFLD; and secondly, to overcome the weight-inducing effect of GLP-1RAs in vivo and to investigate the impact of direct stimulation of the hepatic GLP-1R, whose expression by HepG2 cells has already been established [46]. Here, GLP1R is linked to fatty liver disease.