Thus, in a human del(5q) MDS line, DAB2 knockdown mimics the effects seen in miR-143/145−/−HSPC, suggesting that derepression of DAB2 and TGFβ signaling through depletion of miR-143 and miR-145 in del(5q) MDS may drive HPC expansion while simultaneously suppressing HSC. The gene discussed is DAB2; the disease is myelodysplastic syndrome.