Some studies have pointed out that BAs are FXR receptor agonists and that FXR induces small heterodimer partner (SHP) in the liver and FGF19 (FGF15 in rodents) that bind with liver fibroblast growth factor (FGF) receptor 4 (FGFR4) via an endocrine mode after secretion from the intestine; both signal to inhibit CYP7A1, the rate controlling enzyme in the de novo synthesis of bile acids [17,18,19,20], and restore bile acid homeostasis in models of colitis, thus delaying the pathological progression of colitis [21]. The gene discussed is FGFR4; the disease is colitis.