CML patients displayed inverse expression levels of miR-150 and the transcriptional activator MYB, which correlates with BCR-ABL (fusion gene) transcript levels [44], while down-regulation of miR-10a was associated with increased proliferation by overexpression of the upstream stimulatory factor 2 (USF2) [42]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.