However, except for a few rare genomic rearrangements (MYCN amplification, and CDKN2A deletions), no fusions or other highly recurrent mutations have been identified in other ependymoma groups that could explain their distinct biology, but several recent studies have provided more insight in other oncogenic mechanisms that drive the posterior fossa A ependymomas, which are the focus of this review. This evidence concerns the gene CDKN2A and ependymoma.