TGFBR1 and inflammatory bowel disease: Pathogenic monoallelic variants in TGFBR1/2 as well as in SMAD3 predispose to IBD, strengthening the key role of the SMAD3 canonical pathway for maintaining intestinal homeostasis, a role previously supported by GWAS studies in common multifactorial forms of IBD (1) as well as by Smad3 inactivation in mice (53, 54).