Gal-9 is highly expressed in immune tissues[33], and while engagement of Tim-3 triggers apoptosis in CD4+ Th1 cells[29], T cells and thymocytes[34], this interaction has been suggested to (i) protect activated CD4+ T cells from HIV-1 infection and replication[35], (ii) enhance the production of pro-inflammatory cytokines by immature dendritic cells[36,37] and (iii) regulate the migration of Th2 cells[38]. The gene discussed is HAVCR2; the disease is HIV-1 infection.