Given that mutation of gene encoding adenomatous polyposis coli (APC) is correlated with CRC metastasis through regulating cellular junction and microtubule stability, attachment and migration of CRC cells by binding to β-catenin, tubulin, and GSK-3β [21], it is reasonable to infer that GSK-3β is the junction between insulin signaling and the CRMP2-controlling mechanism, making CRMP2 the link of pathogenesis between CRC and metabolic abnormalities. This evidence concerns the gene DPYSL2 and colorectal carcinoma.