SAXO6 and glioblastoma: These copy number gains contribute to uncontrolled cell proliferation, and are commonly observed events in GBM lesions with MDM1/2/4 amplification found in 15.1% and CDK4/6 amplification found in 15.5% of the TCGA GBM patient cohort.2 The molecular findings in the primary cauda equina GBM are consistent with those observed in previous studies, and add to our understanding of the complex mechanisms leading to GBM tumorigenesis.