Whilst, to date, metabolic changes in reactive astrocytes surrounding CNS tumors have not been investigated, studies demonstrating increased glucose utilization by astrocytes in response to TNF, IL-1β, IL-6, and IFN-γ (Yu et al., 1995; Gavillet et al., 2008; Belanger et al., 2011), and the synergic activity of TNF and IL-1β on astrocyte metabolic activity (Gavillet et al., 2008), suggest that astrocytes in the pro-inflammatory microenvironment will be in a metabolically hyperactive state. This evidence concerns the gene TNF and central nervous system neoplasm.