KLF4 and chronic myelogenous leukemia, BCR-ABL1 positive: 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.