By contrast, overexpressing PHF14 in Calu3 and HCC827 LAD cells significantly enhanced the cell colony formation, invasion and migration abilities of the tested cells treated with TGF-β1, whereas silencing DNMT3B or overexpressing SMAD7 in PHF14-overexpressed cells potently reversed the phenotype synergistically enhanced by TGF-β1 and PHF14 co-expression (Fig. 5g–l), suggesting that the tumor promoting role of PHF14 largely depends on DNMT3B and SMAD7. The gene discussed is PHF14; the disease is neoplasm.