Combining the previous results, the potential mechanism is that KD maintains bile acid homeostasis by increasing efflux, and inhibiting the uptake and synthesis of bile acids via the FXR-mediated induction of BSEP, reduction in NTCP and suppression of CYP7A1, thereby alleviating EE-induced cholestasis and normalizing the expression of metabolic enzyme (SULT2A1) of bile acid in the liver. The gene discussed is SULT2A1; the disease is cholestasis.