All together these findings demonstrate that MEK1/2 can effectively enhance the oncogenic potential of BCR::ABL1 either by directly phosphorylating the fusion oncoprotein at the Y360 and/or Y177 residues [33, 37, 38] or by phosphorylating at the same Tyr residues, and therefore inactivating, its non-mutated counterpart BCR exhibiting tumor-suppressive activities against BCR::ABL1 [30–34]. The gene discussed is ABL1; the disease is neoplasm.