Regardless of the isoform, however, the presence of BCR::ABL1 in malignant cells is highly associated with increased genomic instability due to the cytoplasmic accumulation of reactive oxygen species through the deregulation of the mitochondria membrane potential and with the promotion of non-conservative DNA repair pathways, such as non-homologous end-joining, being responsible for an increase in tumor mutational burden and accelerated leukemic progression [6,7,8]. The gene discussed is ABL1; the disease is neoplasm.