It was shown that germ-free (GF) MyD88-negative non-obese diabetic (NOD) mice develop robust diabetes, whereas NOD.MyD88 (an adaptor for multiple innate immune receptors, TLRs that recognize microbial stimuli)-negative mice with bacterial phyla normally present in the human gut have attenuated T1D [4], suggesting the importance of interplay between commensal gut microbiota and the host for innate immunity. The gene discussed is MYD88; the disease is diabetes mellitus.