The previous observation that inflammation in Il10-/- mice, positive for Helicobacter sp., is abrogated in mice specifically lacking the TLR signaling adaptor MyD88 in mononuclear phagocytes (Hoshi et al., 2012) indicates the likely importance of direct pathogen recognition, including that of Helicobacter sp. and potential other colitis-triggering microbes, for the development of intestinal inflammation in the absence of IL10R signaling. The gene discussed is IL10; the disease is colitis.