The beginning of deciphering these mechanisms started with the identification of the pathogenetic role of the chimeric BCR/ABL oncogene in chronic myeloid leukemia (CML), which arises as a result of reciprocal t(9:22) translocation forming the so-called Philadelphia chromosome [2,3]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.