The increased concentration of Galectin-9 during HIV infection [and more generally during viral infections (68)] supports this hypothesis, where the inhibition of IFN-γ secretion and cytotoxicity occurs through a Tim-3 independent pathway [mediated by cell surface protein disulfide isomerase (69), 4-1-BB (70), or CD44 (71, 72)]. This evidence concerns the gene HAVCR2 and HIV infectious disease.