In line with these observations, trinitrobenzene sulfonic acid (TNBS)- or dextran sodium sulfate (DSS)-induced colitis was ameliorated by administration of siRNA-targeting RIPK2 in NOD2- or NOD1/NOD2-double-deficient mice [17], indicating that the effect of RIPK2 depletion on colitis can occur independently of either NOD1 or NOD2 signaling and TLRs-dependent gut inflammation might be involved. The gene discussed is NOD2; the disease is colitis.