Apparently, infection with EBV results in up-modulation of NKG2DLs, particularly MICB, which is a common cellular defense against viruses mediated by activation of stress response pathways (46) while, analogously to other viruses, EBV has evolved the capacity to contrast cell-surface NKG2DL expression in order to avoid immune recognition, specifically retaining MICB, ULBP2, and ULBP4 into intracellular compartments and inducing the release of sMICB from the cell membrane through the activity of viral factors that are currently unknown. The gene discussed is MICB; the disease is infection.