However, upon antibiotic treatment, MNV infection or sensing of viral ssRNA by TLR7 is able to trigger antimicrobial peptide expression as well as IL‐23 release, and thus tightening of the epithelial barrier together with increased ILC3 function in the defense against vancomycin‐resistant Enterococcus faecium (VRE).119 Interestingly, treatment of psoriasis with the TLR7‐activating drug imiquimod has been linked to colonic dysbiosis and thus to increased susceptibility to DSS colitis.120 However, this was not ILC3 dependent in contrast to reports from the previously discussed study.119. The gene discussed is TLR7; the disease is psoriasis.