Therefore, this low cytotoxic profile observed in non-neoplastic cells reinforces the PARPi specific activity in the exploration of synthetic lethality pathways [67] and corroborates with the proposition that phenotypic alterations associated with the leukemogenesis of BCR::ABL1 p190+ B-cell ALL are determinant factors to the sensitivity to PARPis and not the inherent physiology of B-lymphocytes per se. This evidence concerns the gene BCR and acute lymphoblastic leukemia.