These results indicate that down-regulated activation of RIP2, NF-κB p65, and MAPK p38 in response to stimulation with either the NOD1 agonist Tri-DAP or the NOD2 agonist MDP may be the underlying mechanism(s) responsible for the dysregulated inflammatory response, as represented by attenuated TNF-α and IL-6 production after CPB in pediatric CHD patients. The gene discussed is NOD1; the disease is coronary artery disorder.