In order to evade the tumour suppressive effects of TGF-β1, cancer cells often develop genetic abnormalities within key molecules of the TGF-β signalling pathway, particularly the TGF-β receptors, TGFBR1 and TGFBR2. However, the contribution of alterations in TGF-β receptor expression to the loss of responsiveness towards TGF-β1-mediated growth inhibition in EBV-positive cells is inconclusive. This evidence concerns the gene TGFB1 and neoplasm.