NOD2 mutations engender anti-biotic α-defensin reduction and altered composition of TJ proteins (e.g., claudin-1, claudin-2, occluding, and Zonula Occludens-1), resulting in higher susceptibility to luminal bacterial infection in CD patients (16) and exacerbation of inflammation via interleukin-8 (IL-8)/nuclear factor-κB (NF-κB) activation in epithelia as well as Toll-like receptor-2(TLR2)-dependent interferon-γ (IFN-γ) upregulation in antigen-presenting cells (17, 18). The gene discussed is TLR2; the disease is bacterial infectious disease.