In accordance with the fact that MEK1 can elicit pro-survival signals in the leukemia cells we also found that (ca)MEK1-overexpressing cells were less sensitive to ATO-induced cell death as compared to vector control transfected cells and that genetic disruption of MEK1/2 functions in these (ca)MEK1-overexpressing cells was able to restore their responsiveness to ATO (Fig. 4Ci, Cii and Supplementary Fig. 8). Here, MAP2K1 is linked to leukemia.