BGN and pancreatic neoplasm: We also observed that RAC1B upregulated SMAD3 which in its non-activated form exhibited an anti-migratory effect in pancreatic cancer cells [18] presumably due to its ability to promote the expression of ECAD, via transcriptional induction of miR-200 [19], or biglycan (BGN), a pericellular proteoglycan and potent TGFβ inhibitor [18].