Here, we demonstrated the intracellular mechanisms underlying the anti-proliferative effects induced by AEA in the AGS human gastric cancer cell line, which appear to have been related firstly to a down-regulation of p-AKT and secondly to an up-regulation of p-ERK at times as short as 6 h in both cases, accompanied by the triggering of pro-apoptotic signals and silencing of survival pathways; all effects could be mediated by CB1R and CB2R, without discarding other pathways. This evidence concerns the gene AKT1 and gastric cancer.