VIM and glioma: A surge in neuronal mechanisms such as glial cell differentiation, axon extension, and regulation of myelination and neural precursor cell proliferation was seen due to the enrichment of VIM, SEMA5A, and PTPRZ1. In low-grade glioma, SEMA5A was underexpressed, exhibiting its tumor suppressor nature, but it is compromised in high-grade GBM (X. Li et al., 2012).