In conclusion, we have shown that tolerance to human GBM xenografts in the xenogeneic brain is enabled by a combination of several factors, such as 1) inadequate infiltration of the xenograft tissue and the brain by leukocytes, 2) attenuated systemic levels of pro-inflammatory cytokines, 3) increases in the proportion of Foxp3+ regulatory T cells and reduction in the absolute numbers of Granzyme B+ effector cells and 4) an increase in the levels of tumor-produced immunosuppressive TGF-β2 and decreased levels of leukocyte-attracting chemokines. The gene discussed is TGFB2; the disease is neoplasm.