Therefore, we subsequently evaluated the effects of 17α-E2 treatment in vitro on hepatocytes (HepG2) and hepatic stellate cells (LX-2) and found that 17α-E2 directly mitigates SCD1 production in both cell-types, thereby indicating that 17α-E2 directly signals in both cell-types to suppress drivers of steatosis and fibrosis. Here, SCD is linked to steatosis.