As mentioned in section 1.2.1, intestinal flora homeostasis in DKD patients caused a decrease in the abundance of Bifidobacterium and Lactobacillus, which produce BSH, leading to an obstruction of the dissociation of Tβ-MCA in mice and an increase in the level of Tβ-MCA in vivo, thus increasing the antagonism of FXR. The gene discussed is NR1H4; the disease is diabetic kidney disease.