Perhaps, the combinations of integrin activation, aberrant gene transcription/epigenetic regulation, PTEN loss, and reprogramming of membrane lipid composition additively or synergistically drive the hyper‐activation in FAK or integrin‐FAK/YAP1 axis in CRC, ultimately driving tumor growth, metastasis, and drug resistance in CRC. The gene discussed is PTK2; the disease is neoplasm.