This adds mechanistic insight to previous data highlighting T-cell exhaustion in glioblastoma.18 There was no relationship between CD64 (a receptor required for autoreactive T-cell responses) and CD8+/CD4+ T cells in any area, and no relationship between the antigen presentation/proinflammatory TAM marker HLA-DR and microglial motility (Iba1) in the tumour margins, consistent with a suppressed T-cell response that is likely due in part to a defect in TAM antigen presentation. Here, CD4 is linked to neoplasm.