PXAs also frequently harbor a homozygous deletion of 9p21.3, which includes the tumor suppressor gene CDKN2A. Co-occurrence of BRAF V600E mutations with the CDKN2A deletion incurs poor prognosis because it increases the likelihood of dedifferentiation of PXAs to higher-grade gliomas, typically glioblastomas, as late as 10–20 years after the initial diagnosis [29]. This evidence concerns the gene CDKN2A and central nervous system cancer.