More recently, Sadarangani et al. demonstrated that BC-CML LSC could be targeted using the SMO antagonist PF-04449913, and this acted synergistically with BCR-ABL inhibition to reduce BC-CML LSC survival and self-renewal, likely through downregulation of GLI245. This evidence concerns the gene SMO and chronic myelogenous leukemia, BCR-ABL1 positive.