For example, murine models lacking NOD2, a common target for polymorphism in CD patients, display lower levels of α -defensin secretion compared to wild-type mice.64 This reduction is dependent on the microbiome as Nod2 −/− mice co-housed with wild-type littermates displayed similar levels of α -defensin expression, highlighting the role of the microbiome in disease development.65 Furthermore, the clinical data suggest that the secretion of antimicrobial peptides is altered during CD. This evidence concerns the gene NOD2 and Cowden disease.