According to evidence collected up to now, FOXM1 acts as an absolute oncogene in gliomas, associated with poor survival, independent of the type of cell line, stage of the tumor, etc. The activity of protein kinases such as Akt, MELK, and growth factors (e.g., EGFs or FGFs) subsequently leads to phosphorylation of FOXM1 in gliomas, promoting transcriptional activity of a variety of targets, including STAT3, EZH2, β-catenin, MMP-2, Sox2, VEGF, PDGF-A, VEGF, UBE2C, Rad51, RFC5, BUB1B, Anxa1, SIRT1, ASPM, and ADAM17. This evidence concerns the gene BUB1B and neoplasm.