This hypothesis is supported by the demonstration that Smad7 expression in T cells correlates with disease severity in patients with CD [23] and mice overexpressing sCYLD and Smad7 develop spontaneous colitis due to altered TGF-β signalling and mediated by excessive activation of effector T cells.[23] These latter findings support and expand on data of our previous studies showing that inhibition of Smad7 in the gut of mice with experimental colitis restores TGF-β signalling thus suppressing cytokine responses and limiting the ongoing colitis [24]. Here, TGFB1 is linked to colitis.