This is the case of the employment of the γ-secretase inhibitor DBZ for the conversion of metaplastic Barrett's epithelium into post-mitotic goblet cells76 or in mouse models of familial adenomatous polyposis.77 However, since Hath1 mediates the effects of γ-secretase inhibitor, it has been proposed that only the subset of colorectal cancers that retain Hath1 expression could respond to the treatment.78 This evidence suggests that the pharmacological manipulation of the Notch pathway should be considered with caution and requires an in-depth knowledge of the related context. This evidence concerns the gene ATOH1 and colorectal cancer.