While the histological features of GBM are relatively consistent between different cases, genetic studies revealed the existence of several molecular pathways driving this disease as a function of age and repertoire of oncogenic mutations.92 For example, in younger patients, GBM may be characterized by mutation of the isocitrate dehydrogenase 1 gene (IDH1), which could be coupled with mutation of the TP53 tumor suppressor in the pathway leading to LGG, AA, and secondary GBM. This evidence concerns the gene TP53 and glioblastoma.