The increased sensitivity of most carcinoma cells when compared with normal epithelial cells to autocrine or localized TGFβ signaling [26] and the ability of TGFβ1 to stimulate its own synthesis or increase the number of its receptors on the cell surface [35] may eventually result in a feed-forward loop and a vicious cycle of the TGFβ response [45]. The gene discussed is TGFB1; the disease is carcinoma.