However, DSS administration significantly lowered the NOD1 expression level in the Tibetan group compared to that in the Yorkshire group, indicating that although the “Tibetan microbiota” was likely to activate some of the PRRs under normal physiological conditions, once under the colitis condition, this microbiota suppressed the activation of PRRs and their downstream molecules, including MYD88 and NF-κB. The gene discussed is MYD88; the disease is colitis.