Therefore, a therapeutic approach that inhibits TGF-β signal transduction might turn out to be specifically effective for NSCLC patients with detectable expression of TGFβR2. In fact, blocking TGF-β signal with soluble TGF-β receptor type II protein inhibited TGF-β binding to endogenous TGF-β receptors and reduced tumor cell motility, intravasation, and distant metastasis in a mouse model [29]. Here, TGFBR2 is linked to neoplasm.