In a mouse model of CML, Smo inhibition in hematopoietic progenitors transduced to express Bcr-Abl reduced the extent of disease development and increased disease latency in recipient animals, suggesting that the Smo protein may contribute to the maintenance of a reservoir of leukemia initiating cells [18, 19]. Here, SMO is linked to chronic myelogenous leukemia, BCR-ABL1 positive.