In summary, we have demonstrated that under a hyperlipidemic state, in the absence of SR‐B1, activation of FXR promoted intestinal cholesterol excretion and diminished hyperlipidemia possibly by increasing the expression of cholesterol transporters in ileum to compensate for the loss of SR‐B1‐mediated transhepatic cholesterol movement in mice. Here, NR1H4 is linked to hyperlipidemia.