In addition to the expected GBM signature alterations, GTS identified many CNAs not previously implicated in GBM development, uncovered genomic codeletion of two highly related G1 CKIs, p18INK4C and p16INK4A, in human GBM tumors and cell lines, leading to discovery and validation of a previously unappreciated cell-cycle regulatory circuit in the astrocytic lineage. Here, CDKN2A is linked to glioblastoma.