However, there are two crucial pathways by which HLD induced a higher chance of occurrence of intestinal cancer; either by activating the PPARδ/β-catenin pathway via enhancing the unique differentiating character of the stem cells from normal cells and progression of malignant growth in progenitor intestinal cells [220] or by inhibition of the nuclear bile acid-activated receptor (BAR), farnesoid X receptor (FXR) signaling by reducing bile acid and actively participated in the proliferation of the colonic epithelial cells [221]. This evidence concerns the gene NR1H4 and intestinal cancer.