NR1H4 and congenital secretory chloride diarrhea 1: Considering this finding, PTE regulated FXR activity in the liver of CLD mice through two distinct mechanisms: 1) PTE inhibited macrophage infiltration and activation as well as its-derived inflammatory factor (Figure 3A, Figure 3B, Figure 3C, and Supplementary Figure S1A), resulting in high level of FXR; 2) PTE enhanced SIRT1-mediated deacetylation of FXR (Figure 5C), thereby increasing its DNA binding and associated gene transcription, but SIRT1-mediated FXR deacetylation also led to ubiquitination and proteasomal degradation.