In addition, oral OCA administration improved hepatic steatosis in patients with non-cirrhotic, non-alcoholic steatohepatitis in one clinical trial,(19) and this effect was likely due to inhibition of lipogenesis through the FXR-SHP-SREBP-1c cascade (Fig. 1).(5,6) However, there are no studies on the expression of SREBP-1c-regulated lipogenic genes in the liver tissues of the patients treated with the FXR-ligand. Here, SREBF1 is linked to fatty liver disease.