Abnormal TGFβ signaling in MDS, characterized by reduced (inhibitory) I-SMADs and elevated TGFβ ligands like activin and GDF11, results in the activation of the TGFβ pathway, which impairs late-stage erythropoiesis consistent with morphologic erythroid dysplasia found in most MDS cases (82). Here, GDF11 is linked to myelodysplastic syndrome.