Interestingly, siRNA-mediated knockdown of RIPK2 expression inhibited the development of both DSS- and TNBS-induced colitis in a NOD1/NOD2-independent manner because mice deficient in both NOD1 and NOD2 or in NOD2 only displayed significantly attenuated levels of DSS- and TNBS-induced colitis following the intrarectal administration of the plasmid carrying RIPK2-specific siRNA (Watanabe et al., 2019). Here, NOD1 is linked to colitis.