These results suggested that the ligation of MGr1-Ag/37LRP interaction with its ligand LN initiated FAK phosphorylation and thus activated PI3-K/AKT and MEK/ERK1/2 pathways in GC cells, and the downstream molecule Bcl-2 of both pathways was then upregulated and led to the resistance to apoptosis of adherent GC cells. This evidence concerns the gene AKT1 and gastric cancer.