The progression from low-grade to malignant gliomas involves mutations of the tumor-suppressor gene TP53 and higher expressions of PDGF ligands and receptors; it also involves the accumulation of genetic alterations in retinoblastoma-associated cell-cycle regulatory pathways, including the dysregulation of p16INK4A/CDKN2A or the retinoblastoma susceptibility locus 1 (pRB1), as well as over-expression of cyclin-dependent kinase 4 (CDK4) and human double minute 2 (HDM2). Here, CDKN2A is linked to malignant glioma.