Therefore, it is suggested that GB-neutrophil crosstalk have a prolonged tumor activation that could involve NETs formation and the release of HMGB1, MPO and NE proteins by neutrophils, which activates glioma cells by NFκB signaling, inducing oxidative mutations, impairing mitochondrial function and secreting immunosuppressive cytokines. This evidence concerns the gene NFKB1 and central nervous system cancer.