miR-34a-5p exerts its tumor-suppressive action by targeting and downregulating TGIF2 [85]; TG1F2 constitutes a transcriptional regulator that either binds directly to SMAD genes, recruiting histone deacetylases, or interacts with TGF-β-activated SMADs, repressing SMAD-mediated signaling [86]. This evidence concerns the gene TGFB1 and neoplasm.