The downstream effect of genetic instability in CML leads to the development of ACAs and aberration in both genetic and epigenetic pathways through gene mutations, alteration in tumor suppressor mechanisms, activation of BCR::ABL independent proliferative pathways, and alterations in drug metabolism [37,86,87,88,89]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.