Likely as a result of reduced steatosis and inflammation in the liver, the expression of α-smooth muscle actin (Acta2; −56%),34 which is expressed when resident hepatic stellate cells transform into myofibroblasts upon sensing liver injury and is involved in hepatic fibrogenesis, was lower in the livers of mice treated with combined GIPR/GLP1R agonism as compared to vehicle-treated mice (Fig. 5G). Here, GIPR is linked to steatosis.