These results indicated that the reduced activity of SMAD7, caused by the increased levels of miR-21, was the cause of the overactivation of SMAD2/3 and of the consequent ineffective erythropoiesis in MDS, and that this pathway could be a potential therapeutic target to correct anemia in MDS patients (Figure 2). This evidence concerns the gene SMAD2 and myelodysplastic syndrome.