In this context MEK1/2 protein kinases, key elements of the MEK1/2/BCR::ABL1/ABL1/BCR signaling-centered feedback loop discovered in this study, by activating ERK [55] and inactivating BCR critically contribute to the boosting of Myc protein stability [34] and can therefore also represent a valuable therapeutic target for combination therapies on leukemia patients [36]. The gene discussed is ABL1; the disease is leukemia.