To overcome this limitation and to furthermore rule out the possibility that the transduction procedure or residual NK cell activity of NMRI-Foxn1nu/Foxn1nu mice contributed to the insufficient tumor growth of mock-transduced U251-MG and U251-MGSurvivin cells, we additionally overexpressed mycN, which besides an increased oncogenic signaling induces a metabolic switch to pseudohypoxic glycolysis [60, 68]. This evidence concerns the gene MYCN and neoplasm.