EGFR and colitis: Our observation that iTAP/Frmd8 KO mice exhibit a normal intestinal epithelium under control conditions but are sensitized to DSS-mediated colitis is consistent with the observation that mice homozygous for a hypomorphic mutation of ADAM17 (ADAM17ex/ex) are defective in epithelial repair responses in response to DSS because of a failure to shed EGFR ligands (Chalaris et al, 2010).