Chronic myeloid leukemia (CML) is a clonal disorder originated from hematopoietic stem cells, pathogenically associated with reciprocal chromosomal translocation t(9;22), which gives rise to the fusion gene BCR-ABL, encoding for a protein of p210 kDa with a constitutively activated tyrosine kinase (TK) activity [1, 2]. The gene discussed is TKT; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.