As described above, imatinib blocked the activity of tyrosine kinases and the expression of phospho-Crkl, induced by the de novo BCR/ABL protein caused by K562 EVs bearing BCR/ABL DNA, indicated that the de novo BCR/ABL protein is taken in the pathogenesis of CML. This evidence concerns the gene CRKL and chronic myelogenous leukemia, BCR-ABL1 positive.