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Normal epithelial thyroid cells in culture are inhibited by TGF-𝛽1. Instead, transformed thyroid cell lines are frequently resistant to its growth inhibitory effect. Loss of TGF-𝛽 responsiveness could be due to a reduced expression of TGF-𝛽 receptors, as shown in transformed rat thyroid cell lines and in human thyroid tumors, or to alterations of other genes controlling TGF-𝛽 signal transduction pathway. However, in thyroid neoplasia, a complex pattern of alterations occurring during transformation and progression has been identified. Functionally, TGF-𝛽1 acts as a tumor suppressor in the early stage of transformation or as a tumor promoter in advanced cancer. This peculiar pleiotropic behaviour of TGF-𝛽 may result from cross-talk with signalling pathways mediated by other growth factors, among which EGF-like ligands play an important role. This paper reports evidences on TGF-𝛽1 and EGF systems in thyroid tumors and on the cross-talk between these growth factors in thyroid cancer.