The hybrid BCR-ABL gene and its tyrosine kinase constitutionally active recombinant fusion protein (p210 BCR-ABL) deriving from the reciprocal translocation between chromosomes 9 and 22 is associated with the clinical development of chronic myeloid leukemia (CML).1–2 This fusion results in the expression of two forms of protein-tyrosine kinases: p190 (BCR-ABL) and p210 (BCR-ABL) with subsequent dysregulation of intracellular signaling that drive cells to enhanced proliferative capability and resistance to apoptosis. This evidence concerns the gene EVPL and chronic myelogenous leukemia, BCR-ABL1 positive.