In vivo studies have confirmed that DCLK1 plays an oncogenic role in tumor initiation, proliferation, and quiescence due to activation of Wnt and Notch1 signaling pathways in addition to stimulating inflammation in mouse models of colon cancer [12, 16, 18, 20, 22, 44]; the antibodies used in these experiments could recognize the similar epitopes of both DCLK1-L and DCLK1-S isoforms. Here, NOTCH1 is linked to neoplasm.