Studies with mice deficient of TLRs, ILRs, MyD88, or Tir8/Sigirr suggest that a fine balance of pro- and anti-inflammatory signals induced by commensal bacteria through TLRs- or ILRs-signaling is necessary for the homeostatic regulation of colon epithelium proliferation and apoptosis as well as for inflammatory responses, mechanisms of repair, and colitis-associated tumorigenesis (Rakoff-Nahoum et al., 2004; Araki et al., 2005; Salcedo et al., 2010). Here, SIGIRR is linked to colitis.