While mutation-driven RAS activation governed cellular response to pyrvinium in minimal cellular models, the effect of pyrvinium—or to trametinib—was not selective for RAS mutated AML samples, but dependent on RAS signaling pathway activation, as illustrated by the sensitivity of FLT3-mutated AML to MEK inhibitors or to pyrvinium [53, 54]. Here, FLT3 is linked to acute myeloid leukemia.