In the aggressive neuroblastoma cell line BE(2)-C, which possesses GRPR, the knockdown of GRPR resulted in a decrease in DNA synthesis, a cell cycle arrest at the G(2)/M phase, a decrease in cell proliferation, a change in cell morphology, and a downregulation of p-AKT, a crucial driver in cell survival and development of cell metastases (190, 199). This evidence concerns the gene AKT1 and neuroblastoma.