BCL-2 activity is directly controlled by AKT/mammalian target of rapamycin (mTOR) signalling, and a combination of crizotinib with mTOR inhibitor Torin2 prolonged survival of mice with ALKF1174L/MYCN NB tumours, which overexpress BCL-2 and are resistant to crizotinib [280]. This evidence concerns the gene AKT1 and neuroblastoma.