CTLA4 and glioblastoma: In turn M1 to M2 polarization may enhance the expression and functional activity of events and may create a milieu favoring immune escape also from upregulated expression of immune checkpoint inhibitors such as cytotoxic T lymphocyte-associated antigen 4 (CTLA4) and programmed cell death (PD)-1 that ultimately generate a local pro-oncogenic milieu favoring immune evasion and growth of GBM [9].