We find, therefore, that the GBM-specific amplifications, of AKT3, HRAS, and genes involved in decreased Rb activity, together with the LGA-shared deletions of CDKN2A and CDKN2B, and CNAs involved in decreased activity of p53, enhance the opportunity for human normal to tumor cell transformation in response to growth factor signaling in GBM relative to LGA. The gene discussed is CDKN2B; the disease is glioblastoma.