AMPAR-mediated tumor proliferation seemed to involve a Ca2+-dependent activation of Akt/PKB signaling pathway [44], since both NBQX (AMPAR antagonist) and Wortmannin (specific inhibitor of PI3K) reduced the Akt/PKB phosphorylation and decreased the number of tumoral viable cells in culture [45]. This evidence concerns the gene AKT1 and neoplasm.