The higher expression of PD-L1 on B cells in HIV infection raises the possibility that these CD19+PD-L1+ B cells may be interacting with T cells through PD1, contributing to the development of AIDS-NHL by inhibiting/impairing CD4+ and CD8+ T cells, which play an important role in dampening the growth of EBV-infected B cells and which can effect anti-tumor responses (Fig. 5). The gene discussed is CD8A; the disease is non-Hodgkin lymphoma.