In GBM, the resulting phenotype can inhibit immune response through secretion of transforming growth factor β1 (TGFβ1), arginase 1 (ARG1), or interleukin 10 (IL-10) enhancing neo-angiogenesis through VEGF production and extracellular matrix modeling by metalloproteases (MP) (38). This evidence concerns the gene TGFB1 and glioblastoma.