lnc-TSI specifically inhibited Smad3 phosphorylation by binding with the MH2 domain of Smad3 to block the interaction between Smad3 and TβRI, suggesting that upregulation of lnc-TSI in ccRCC cells might be a self-protective mechanism for tumor metastasis and could serve as a therapeutic target. This evidence concerns the gene SMAD3 and neoplasm.