Mechanistically, we determined that pyrvinium predominantly inhibited mitochondrial oxydative phosphorylation in RAS+ AML, as observed in other cancers and in FLT3-mutated AML [54, 61–63], and this mitochondrial dependency is further illustrated by the anti-leukemic activity of the mitochondria uncoupling agent niclosamide in RAS+ AML cells, as recently demonstrated in T-ALL [64]. The gene discussed is FLT3; the disease is acute lymphoblastic leukemia.