In our study, the effect of Malat1 on IL-10 expression is observed both in in vitro differentiated Th cells and in vivo in two distinct infection models progressing at significantly different timescales (days for PcAS versus weeks for L. donovani), demonstrating a CD4+ T cell–intrinsic regulatory role for Malat1. We note that because of the use of a full Malat1−/− mouse, we cannot exclude other CD4+ T cell–independent mechanism contributing to L. donovani clearance or PcAS-induced immunopathology. The gene discussed is IL10; the disease is infection.