These findings establish an LMP1-JunB-p18<sup>INK4c</sup> axis as essential for EBV- driven lymphoblastoid B cell proliferation, suggest JunB-mediated cross-talk between Epstein-Barr nuclear antigens and LMP1, and highlight JunB as a potential therapeutic target for EBV-associated lymphoproliferative disorders. The gene discussed is CDKN2C; the disease is lymphoproliferative syndrome.