For instance, inhibition of γ-secretase, which is a key component in the Notch extra-cellular signal transduction pathway showed significant anti-tumor activity in patients desmoid tumors (ORR 71.4%) in a phase I trial.[102, 103] CTNNB1 mutations are observed is as much as 85% of desmoid tumors, which may indicate potential interactions between the Notch and Wnt/β-catenin pathways.[104]. Here, CTNNB1 is linked to desmoid tumor.