The molecular mechanism involved inhibition of the DNA-binding activity of the Smad3/4 transcription factor complex, through a direct interaction between the central domain (amino acids 59–126) of tumor-derived core and the MH1 DNA-binding domain of Smad3, thus preventing its binding to DNA, and presumably promoting cell transformation by providing, to clonally expanding cells, resistance to TGF-beta antiproliferative effects. Here, SMAD3 is linked to neoplasm.