Concerning CNS tumors other than HGG, aggregated molecular evidence points towards the fusion of zfta or yap1 genes in the development of supratentorial ependymomas; h3, ezhip, or tert mutations in some infratentorial ependymal tumors; mycn amplifications in spinal ependymomas, in addition to the previously known mutations in nf2 [12,13]. This evidence concerns the gene MYCN and ependymal tumor.