Since it is generally believed that autophagy contributes to stemness maintenance of CSCs [15] and increases in Dclk1 correlates with the malignant status and poor outcome in malignant tumors [24], our studies provide a rationale to capture these interactions early through small molecule inhibitor-based Dclk1 targeting to block Dclk1 from interacting with p62 as a strategy to prevent or treat colon cancer. This evidence concerns the gene SQSTM1 and colonic neoplasm.