Examination of several signaling pathways revealed a striking elevation of p-AKT protein in Sesn1+/+-BDL, which was greatly dampened in Sesn1−/−-BDL livers (Fig. 4C left and Fig. 4D left), suggesting that SESN1 contributed to AKT activation in cholestasis. The gene discussed is SESN1; the disease is cholestasis.