Furthermore, overexpression of miRNA-409-5p improves imatinib-induced proliferation inhibition and cell cycle arrest.63 Recently, in a study of miRNome profiling of LSC from CML-CP patients revealed a nine-fold increase of miR-196a-5p in CD34+CD38−CD26+ (BCR-ABL+) compared to CD34+CD38−CD26- (BCR-ABL-).64 Amplification of BCR-ABL and increased Jak2 signaling activate ADAR1, a double-stranded RNA protein that mediates adenosine to inosine (A-to-I) editing, thereby enhance the capacity of CML-LSC renewal by impairing the biogenesis of the Let-7miRNA family.65 The gene discussed is ADAR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.