As expected, blockade of the activation of EGFR as well as PI3K/AKT signaling by their respective pharmacological inhibitors eliminated the discrepant capacities in proliferation and invasion between control and CHKA-silenced cells; conversely, activation of AKT signaling by ectopic expression of myr-AKT effectively reversed the inhibitory effects of CHKA knockdown on CRC cell proliferation and invasion. The gene discussed is AKT1; the disease is colorectal carcinoma.