Future studies should be aimed at examining whether Gal-1 may serve as a compensatory mediator that controls resolution of inflammation during HIV-1 infection, similar to its role in models of neuroinflammation (42) or sialadenitis (75), or whether it may act as an alarmin, thus amplifying inflammatory responses and recapitulating its early role in sepsis (44). This evidence concerns the gene LGALS1 and Sepsis.