Mechanistically, RAC1B-dependent protection from mesenchymal conversion and acquisition of a motile phenotype was due to suppression of tumor-promoting MEK-ERK2 signaling [15,16] and interference with TGFβ1 signaling via downregulation of the TGFβ type I receptor ALK5 [4] and induction of the inhibitory Smad, SMAD7 [17]. This evidence concerns the gene TGFB1 and neoplasm.