Overall, our results reveal that in CML cases with variant t(9;22) there is an enhancement of the MAPK pathway deregulation already known to underlie the CML pathogenesis and point out the role of interesting candidate genes, such as TRIB1, PTK2B, and C5AR1. These findings show that kinases are a common target of molecular alterations in hematological disorders and reinforce the idea that a perturbed action of signal transduction pathways is one of the hallmarks of cancer. Here, TRIB1 is linked to hematologic disorder.