The likely contribution of SMAD7 activation to the observed TGF-β pathway inhibiton in CML LSCs compared to normal HSCs and the current clinical investigation of antisense oligonucleotides for SMAD7 inhibition in Crohn's disease[44] make it an attractive target for CML LSC-directed therapy. The gene discussed is SMAD7; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.