Cells chronically infected with herpes virus (cytomegalovirus (CMV) and EBV) and malignant cells employ mechanisms of immune evasion, such as alterations in the CD279/CD274 signaling pathway and the interaction of CD70 with CD27.27, 28 In mouse melanoma models, anti-CD27 treatment correlated to lower CD279 expression on CD8+ T cells. This evidence concerns the gene CD274 and melanoma.