MSH6 is an essential component of the DNA mismatch repair mechanism and has been proposed to interact as an epigenetic regulator.32 Loss-of-function mutation was reported in relapsed ALL patients33 and the mutation leads to constitutional mismatch repair deficiency syndrome, which is characterized by the development of childhood cancers, mainly hematological malignancies.34 Taken together, epigenetic regulation may play important roles against the etiology of CML. Here, MSH6 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.