“…In support of this suggestion, expression studies revealed that BCR-ABL1 dramatically perturbs the CML transcriptome (31), resulting in altered expression of genes, some of which (e.g., PRAME, MZF1, EVI-1, WT1, and JUN-B) might play a role in BP (19,(32)(33)(34). Nonetheless, the posttranscriptional, translational, and posttranslational effects of high BCR-ABL1 levels result in the constitutive activation of factors with reported mitogenic, antiapoptotic, and antidifferentiation activity (e.g., MAPK ERK1/2 , MYC, JAK2, YES-1, LYN, hnRNP-E2, MDM2, STAT5, BMI-1, and BCL-2) and inhibition of major key regulators of cellular processes, such as those regulated by the tumor suppressors p53, CCAAT/enhancer binding protein-α (C/EBPα), and PP2A (19,29,35). Interestingly, a signature based on six genes (NOB1, DDX47, IGSF2, LTB4R, SCARB1, and SLC25A3) was recently found to accurately discriminate early from late CP, CP from AP, and CP from BP (36); however, the biological role of these genes in disease progression is still unknown.…”