In the classical example of CML, the BCR::ABL1 fusion gene encodes a multi-domain, constitutively active chimeric tyrosine kinase [13], in turn activating downstream signaling pathways that result in abnormal cellular adhesion, inhibition of apoptosis through inactivation of tumor suppressor genes [14,15], and eventually, uncontrolled proliferation of myeloid cells. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.