Gregory et al. performed a synthetic lethality screen in AML cell line MOLM13 harboring a FLT3-ITD mutation and found that a number of the genes able to sensitize AML FLT3-ITD cells to FLT3 inhibitors were involved in metabolic processes [183], in particular the ataxia telangiectasia mutated (ATM) gene shown to activate G6PD to maintain redox homeostasis [184]. This evidence concerns the gene ATM and acute myeloid leukemia.