Lastly, mapping of synergism and resistance predictions onto known FLT3 signaling cascades in AML [22] highlights the dependence of FLT3-ITD AML on enhanced downstream MAPK signaling, and predicts that deactivating Ras mutations would promote synergy; this is in line with recent work showing that activating Ras mutations can promote FLT3 inhibitor resistance clinically (Figure S2) [23]. The gene discussed is FLT3; the disease is acute myeloid leukemia.