Knockdown of these two genes synergistically restored TGF-β responsiveness in gastric cancer cells and reduced tumor growth in vivo; biochemical analysis demonstrated that MEL1/PRDM16 interacted with SKI and inhibited TGF-β signaling by stabilizing the inactive Smad3-SKI complex on the promoter of TGF-β target genes (Figure 3D) [251]. Here, PRDM16 is linked to neoplasm.