Recent studies have suggested that several alterations promote this progress, including differentiation arrest caused by the suppression of translation of the transcription factor CEBPα induced by the BCR-ABL oncoprotein in CML cell, increasing genomic instability in CML cell resulting from the reduced capability of genome surveillance system, telomere shortening and loss of tumor suppressor gene (TSG) such as TP53, retinoblastoma 1, CDKN2A, DAPK1 and others [16,26,27]. This evidence concerns the gene CEBPA and chronic myelogenous leukemia, BCR-ABL1 positive.