EBV-specific human T cells express CD27 and homozygous mutations in CD27 resulting in CD27 deficiency are associated with persistent EBV viremia, suggesting that the CD27/CD70 axis plays an important role in the control of EBV infection.42, 43 It is well possible that the high CD70 expression by the EBV B-LCLs, which is confirmed by our RNAseq data, supports immune escape, as seen in human glioblastomas and in lymphoproliferative diseases.44 Other evidence indicates that the CD27/CD70 pathway plays an important pro-pathogenic role in autoimmune conditions. This evidence concerns the gene CD27 and glioblastoma.