In this context, it has been recently shown that a short natural splice form of the deubiquitinating enzyme CYLD (sCYLD), a tumour suppressor that is mutated in patients with familial cylindromatosus, interacts with Smad7 in the nucleus of CD mucosal T cells, where the complex inhibits the binding of Smad3 to the DNA, thereby abrogating TGF-β activity. Here, CYLD is linked to neoplasm.