Finally, the close association of RAC1B expression with a differentiated epithelial phenotype and tumor-suppressive Smad signaling on the one hand and its low or absent expression in undifferentiated mesenchymal-type tumor cells with tumor-promoting non-Smad, i.e., ERK signaling on the other hand corresponds well to the function of TGFβ as a tumor suppressor in early-stage cancers and a tumor promoter in their late-stage counterparts, the shift of which is known as the “TGFβ paradox” [114,115]. Here, TGFB1 is linked to neoplasm.