FXR deficiency results in enhanced tumor development in APCMin/+ mice (140), whereas adenoviral-mediated overexpression of constitutively active FXR in HT29 xenografts inhibits tumor growth via the induction of the proapoptotic FAS, BAK1, p21, KLF4, FADD, CASP9, and p27 genes; and downregulation of antiapoptotic BCL2 and proinflammatory TNFα (141). Here, FADD is linked to neoplasm.