When considering our data and the study of Kim et al. [15], we suggest a model for the role of TGF-β in gastric carcinogenesis, whereby TGF-β1 signaling changes from the tumor-suppressive Smad-dependent pathway to a tumor-activating Smad-independent pathway as the cancer progresses, irrespective of histologic subtypes of gastric cancer. This evidence concerns the gene TGFB1 and neoplasm.