Pericytes interacting with GBM acquire an anti-inflammatory phenotype, increasing the expression of IL-10, TGF-β, IL-1, IL-23, IL-12, and IL-6, accompanied by a decreased expression of co-stimulatory molecules such as CD80 and CD86 and a reduction in the expression levels of major histocompatibility complex class II (MHC-II) molecules, suggesting impaired antigen presentation ability by GBM-pericytes. This evidence concerns the gene TGFB1 and glioblastoma.