Further supporting this model, tagging GFP to the endogenous c-Myc locus in KLF4-deficient CML LSCs showed a significant reduction in GFP-cMYC, and ectopic expression of a c-MYC mutant with an amino acid substitution at position 62 (Ala for Ser) restored the progression of CML disease in mouse models14. This evidence concerns the gene MYC and chronic myelogenous leukemia, BCR-ABL1 positive.