Inhibition of AKT in LUAD cells with either low or high CCT3 expression showed that cell proliferation was more significantly suppressed in CCT3-overexpressing cells.[31] Bioinformatic analysis further revealed that the PI3K/AKT/mTOR signaling pathway is associated with CCT3 expression in head and neck squamous cell carcinoma cells.[63] Taken together, CCT3 may influence tumor progression through the AKT/mTOR signaling pathway and represents a potential therapeutic target for cancer treatment. This evidence concerns the gene AKT1 and cancer.