Both proteins are crucial downstream effectors of tyrosine kinase oncogenes (TKO) such as Fms-like receptor tyrosine kinase 3 with internal tandem duplications (Flt3-ITD), BCR-ABL and JAK2V617F which cause AML, CML and other myeloproliferative diseases (MPD), respectively [1]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.