The life cycle of Epstein–Barr virus (EBV) is intriguing in that the virus resides within the immune system and utilizes distinct latency expression programs to establish a persistent infection yet escaping elimination. To achieve this EBV has hijacked cellular signaling pathways to its own benefit, but deregulated viral gene expression can turn into oncogenesis. EBV like many other persistent herpes viruses has evolved ingenious tricks to evade the immune system in part by mimicking host gene function(s). Latent membrane protein 1 (LMP1) mimics CD40 signaling as part of its “normal” biological function and when deregulated, functions as a viral oncogene. LMP1 also affects cell–cell contact, cytokine and chemokine production, Ag presentation and is secreted in the extracellular milieu via immunogenic exosomes. Thus, besides its well-known growth promoting properties LMP1 modulates immune responses. Herein we discuss current knowledge regarding the role of LMP1 in immune evasion of EBV and how this strategy for establishment of persistence contributes to immune escape of EBV+ tumors.