That some indexes of CDD-induced low-grade inflammation, particularly colon shortening, were ameliorated in MyD88-deficient mice suggests a role for TLR-mediated detection of bacterial products in driving such low-grade inflammation, which is in accord with work of Cani and colleagues that TLR-4 drives HFD-induced metabolic syndrome (5). The gene discussed is MYD88; the disease is craniodiaphyseal dysplasia.