Although much have been reported on the presence of genetic alterations in TP53, PTEN, and CDKN2A genes in several tumor types, few studies have focused on the analysis of the incidence of co-alterations of these three genes, through different types of mechanisms which lead to loss of protein function, such as mutations and deletions, in a single sample of gliomas. The gene discussed is CDKN2A; the disease is neoplasm.