It has been reported [40] that AA also induced apoptosis in non-small cell lung cancer cells (A549) by inhibiting COX-2 activity, which in turn down-regulated the PI3K/AKT/mTOR signaling pathway and inhibited the migration of the cancer cells in a concentration-dependent manner, and the 24-h migration rate of AA-treated (15, 30, 60 μM) A549 cells (71.02%, 44.05%, 19.34%) was significantly reduced compared to untreated cells (85.2%). The gene discussed is AKT1; the disease is cancer.