In mice with APC gene silencing mutation (Apcmin/+) or those treated with the colon chemical carcinogen azoxymethane (AOM)/dextran sulfate sodium (DSS), FXR loss promotes intestinal tumor progression and an increased adenoma size, which leads to early mortality, while the transgenic overexpression of FXR in gut cells reduces tumor growth and development [113,118]. This evidence concerns the gene NR1H4 and intestinal neoplasm.