The current study indicates that both FAK and PYK2 are elevated in already established colon tumors in CRC patients and that effective inhibition of the Wnt/β-catenin pathway in CRC cells expressing FAK and PYK2 will only be achieved by simultaneously targeting both kinases; we believe these results provide a solid mechanistic justification for clinical use of FAK/PYK2 dual inhibitor instead of FAK-specific inhibitor for better clinical outcomes in CRC patients. This evidence concerns the gene PTK2 and colonic neoplasm.