Large-scale genomic analyses of human glioblastoma have identified numerous mutated genes, and the data propose that three core signaling pathways are altered in the majority of the tumors: the receptor tyrosine kinase (RTK)/RAS/PI3K pathway, where EGFR amplification, PDGFRA overexpression or amplification, and PTEN inactivation are among the most common mutations; the p53 pathway, where inactivation of p53 and p14Arf are key events; and the RB pathway, with inactivation of RB and p16Ink4a as the most frequent alterations (1,2). This evidence concerns the gene CDKN2A and glioblastoma.