Souza CA, Pagnano KB, Bendit I, Conchon M, Freitas CM, Coelho AM, Funke VA, Bernardo WM the presence of 1% to 19% blasts in the blood or bone marrow, basophils > 20%, thrombocytosis or thrombocytopenia not related to therapy and clonal evolution in cytogenetic evaluation. The blast crisis phase is characterized by blasts > 20% of peripheral blood white cells or extramedullary blast proliferation(1-3)(D). Recommendation: Diagnosis of CML depends on the identification of the Philadelphia chromosome or the BCR-ABL rearrangement. Is there any difference in the prognosis of CML patients with p210 e13a2(b2a2) and e14a2(b3a2) or (e1a2) p190 rearrangements? The prevalence of the e1a2 BCR-ABL fusion transcript in CML patients is 1%. This rearrangement is associated with decreased therapeutic response to tyrosine kinase inhibitors (TKIs) as complete hematologic response is attained in only 30% of cases, complete cytogenetic response in 20% (3 to 18 months) and major molecular response in 10% of cases. Progression to other phases (accelerated or blast crisis) occurs in 60% of chronic phase patients(4)(C). The response of treatment-naïve CML patients to imatinib treatment is different for the b3a2(e14a2) and b2a2(e13a2) transcripts. In 12 months of treatment, patients with the b3a2(e14a2) transcript have a 29% increase in complete cytogenetic response, which is faster, and greater disease-free survival(5)(B). In CML patients on imatinib treatment for six months, the number of b2a2(e13a2) transcripts is lower when compared to the number of b3a2(e14a2) transcripts, suggesting greater sensitivity of the b2a2(e13a2) transcripts to imatinib and consequently prognosis is better(6)(B). Imatinib treatment in chronic-phase CML patients with the BCR-ABL b2a2(e13a2) transcript has better results compared to those with the b3a2(e14a2) transcript with a 31% increase in the major cytogenetic response and a smaller number of BCR-ABL transcripts(7)(B). Recommendation: the (e1a2)p190 transcript is associated to a reduced therapeutic response; there is controversy as to whether there is difference in response between the p210 e13a2(b2a2) and p210 e14a2(b3a2) transcripts. At diagnosis, do the Philadelphia chromosome and 9q deletion have prognostic significance? There is no difference in survival between CML patients with the chromosome 9q deletion on interferon alpha treatment and those without this deletion. However, there is a reduction in the survival of patients with the deletion spanning the BCR-ABL junction compared to those without this deletion. The survival rate is 44% higher in chronic phase patients submitted to bone 368 marrow transplantation who do not have the deletion (Number needed to treat - NNT: 2)(8)(B). There is evidence that the disease-free survival, overall survival and cytogenetic response is reduced in CML patients with the chromosome 9q34 deletion under treatment with interferon alpha(9,10)(B). A comparison of first-generation (imatinib) or second- generation (nilotinib or dasatinib) TKIs in the treatment of CML patients with chromosome 9 deletion shows that there is no significant difference in the overall survival, disease-free survival or in cytogenetic response between patients with and without the chromosome 9 deletion over a two-year follow-up(11,12)(B). There is, however, evidence that there is a reduction in survival of patients with derivative chromosome 9 deletions(13)(B). The ABL deletion on derivative 9 (15.1%) in CML patients reduces disease-free survival, the BCR deletion reduces overall survival and combined ABL and BCR deletions reduce the overall and disease-free survival(14,15)(B). There is evidence that only the ABL deletion reduces the survival time and the duration of the chronic phase(16)(B). Over a 5-year follow up of imatinib treatment, CML patients with variant Philadelphia chromosome translocations do not demonstrate significant differences in overall survival, disease-free survival, progression-free survival, complete hematological response, cytogenetic response or molecular response compared to patients without variant Philadelphia chromosome translocations(17,18)(B). Other studies have shown that Philadelphia chromosome mosaicism increases mortality in 3.3 years by 21% (NNH: 5) and translocation variations reduce cytogenetic response(19,20)(B). Recommendation: Despite controversy on whether chromosome 9q, BCR deletions and variant Philadelphia chromosome translocations confer worse prognoses, there is evidence of reductions in overall and disease- free survival and in therapeutic response of CML patients treated with interferon alpha or first-generation and second-generation TKIs. ABL deletion reduces the overall and disease-free survival of patients. The presence of variant Philadelphia chromosome translocations and mosaicism also seem to confer worse prognosis in CML. Do cytogenetic abnormalities in addition to the Philadelphia chromosome at diagnosis have prognostic significance? In CML patients under treatment using first-generation (imatinib) and second-generation (dasatinib or nilotinib) TKIs, the presence of additional chromosomal abnormalities reduces disease-free and overall survival at 5 years(21)(B). The presence of additional chromosomal aberrations in CML patients under treatment with nilotinib increases mortality by 28% due to disease progression (NNH: 4). In addition, mortality is increased by 38% at 2 years in chronic phase patients with additional chromosomal aberrations (NNH: 3)(22)(B). Aberrations reduce the survival time of these patients(23,24)(B). The presence of additional chromosomal aberrations increases Rev Bras Hematol Hemoter. 2012;34(5):367-82