Our findings support a model that up-regulation of Slit2 directly results in the recruitment of the adaptor protein Robo1, which then phosphorylates Src and suppresses the expression of E-cadherin, leading to an increased activity of Wnt/β-catenin signaling, and thereby promotes the tumor growth and accelerates the progression of the intestinal tumors (Figure 6). The gene discussed is SRC; the disease is intestinal neoplasm.