This increased lytic EBV replication may both promote the suppression of EBV-specific immune control via viral IL-10 (BCRF1) [62] and generate higher frequencies of Burkitt’s lymphoma precursors that, via EBNA3C-mediated AID expression, may allow for the c-myc translocation that is characteristic of Burkitt’s lymphoma (Table 1) [39]. Here, MYC is linked to Burkitt lymphoma.