Nevertheless, the relatively high gene dosage of hCINAP in cancer cells suggests that human cancer cells may have a tendency to overexpress hCINAP. The remarkable inhibitory effect of hCINAP depletion on tumorigenesis demonstrates that exploration of upstream regulators of hCINAP and generation of selective small-molecule inhibitors targeting hCINAP may provide therapeutic strategies for patients with cancer. Here, AK6 is linked to cancer.