Targeting additional components of the faulty CML DNA repair pathways, for example, by inhibiting the essential DNA repair factor PARP1, could constitute a helpful therapeutic strategy to be exploited by single or combined treatments, especially as PARP1 and DNA ligase IIIα levels were described as biomarkers in resistant CML patients. This evidence concerns the gene PARP1 and chronic myelogenous leukemia, BCR-ABL1 positive.