From a therapeutic perspective, blocking release of p/mTGF-β1, or promoting the generation of aTGF-β1, by targeting L-TGF-β1 through modulation of CER could be exploited to interfere with epithelial–mesenchymal transition, a developmental programme employed by TGF-β1 to promote carcinoma progression5 (Fig. 1b), while analogous targeting of L-MSTN may cure cancer-associated cachexia. Here, TGFB1 is linked to carcinoma.