As ABL1 may exhibit both pro- and anti-apoptotic functions depending on its nuclear vs. cytoplasmic localization [18, 19, 26, 27] and its intracellular localization is regulated by phosphorylation of its Thr735 residue which promotes cytoplasmic sequestration by the 14-3-3 protein [28], we explored whether MEK1/2 inhibition also affected Thr735 phosphorylation and/or the subcellular localization of ABL1 in leukemia cells. The gene discussed is ABL1; the disease is leukemia.