Several studies have indicated that the immunosuppressive tumor microenvironment of GBM enhances the induction of tumor-associated macrophages, regulatory T cells, and immunosuppressive molecules such as PDL1, TIM-3, LAG-3, TIGIT, CD137, CD47, and CTLA4, allowing the GBM tumor to escape the antitumoral functions of T and NK cells (9, 10). This evidence concerns the gene HAVCR2 and neoplasm.