Importantly, virtually all cells of the innate and adaptive immune system can secrete IL-10.1,5 However, various murine T cell-specific knock-out models have established non-redundant functions for CD4+ T cell-derived IL-10 in maintaining immune homeostasis to intestinal commensal microbes and during the resolution phase of pathogen infections.2 Indeed, CD4+ T cell-specific loss of IL-10 in mice is sufficient to cause spontaneous development of intestinal inflammation.6,7. The gene discussed is CD4; the disease is inflammation.