1. Pathway switch from AP1-regulated clone at diagnosis to mTOR-driven clone at relapse in DNMT3A/FLT3-ITD AML2. Shared LSC signature between diagnosis and relapse in two ETO-AML cases3. Tumor heterogeneity among patients with similar initiating mutations, also between each diagnosis-relapse pair. This evidence concerns the gene MTOR and acute myeloid leukemia.