The therapeutic efficiency obtained in our patient may be explained by the sensitivity of cell lines to the action of ABL inhibitors [13], and the use of bevacizumab, a monoclonal antibody to vascular endothelial growth factor (VEGF) which potentiates the action of imatinib, was like that described in many solid cancers, and inhibits VEGF involved in the initiation and development of CML [15]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.