Combining the genomic and functional characterization of these different fractions, we modeled the leukemogenesis in this patient, originating from preleukemic CH-containing TET2/TP53 mutant HSCs, which give rise to TIM3+ LSCs with heightened self-renewal capacity, driving AML with heterozygous TET2/TP53 mutation status (Fig. 5G). The gene discussed is TP53; the disease is acute myeloid leukemia.