“…This translocation gives rise to chimeric fusion proteins, collectively named BCR-ABL1, whose constitutively activated tyrosine kinase activity is ultimately responsible for the altered differentiation, uncontrolled replication, and resistance to apoptosis typically displayed by CML cells. Most CML patients present a BCR-ABL1 fusion downstream of exons 13 and 14 of the BCR gene, originating transcripts with an e14 and/or an e13 junction, which drive the expression of a 210 kDa chimeric protein designated p210 BCR-ABL1 (M-BCR), although other isoform fusion proteins (namely p190 and p230) have also been described at lower frequencies in some patient subtypes [ 2 , 3 , 4 , 5 , 6 ]. The enduring proliferation of CML stem cells expressing BCR-ABL1 fusion proteins eventually potentiates the occurrence of additional mutations, which are often associated with a more negative prognosis and the eventual development of resistance to clinical treatments [ 7 , 8 ].…”