Zanoni et al. have shown the RV infection to be a potential trigger for the onset of CD.24 They demonstrated that a subset of anti-TG IgA antibodies recognize a RV viral protein, VP7, and such antibodies increase small intestine permeability and induce monocyte activation.24 However, a cohort study conducted in the USA found that frequent clinically asymptomatic RV infections in children with human leukocyte antigen (HLA) risk alleles for CD lead to a higher risk for CD autoimmunity.25 Viruses other than RV have been implicated in the pathogenesis of CD. The gene discussed is CD79A; the disease is Cowden disease.