The increased availability of TGF-β ligands in tumors, particularly TGF-β1 (expressed by tumor cells, stromal elements, or released by platelets) coupled to the reduced sequestration of TGF-βs by EMC proteins such as decorin, and the enhanced activation of TGF-βs by factors such as proteases, integrins, and TSP-1, drives TGF-β signaling in tumor cells despite the loss of TGF-β receptor numbers. This evidence concerns the gene TGFB1 and neoplasm.