(G) Kaplan-Meier survival plot of secondary mice transplanted with primary inv(16)/Tet2-/- AML cells (2° AML, n = 6 per group, transplanted with GFP+ AML cells from early, median and late AML. (B) Kaplan-Meier plot showing overall survival of primary mice developing overt AML (1° AML) after transplantation of inv(16)/Tet2-/- AML cells (n = 12). Acute myeloid leukaemia (AML) represents an aggressive cancer entity, which develops through clonal evolution, propagated by accumulating independent somatic molecular and chromosomal aberrations in haematopoietic stem and progenitor cells (HSPCs).1 Consistent with the significant heterogeneity and complexity of AML genomes, AML patients demonstrate highly variable response rates and overall survival when treated with conventional therapeutic regimens. Overall, analyses of DEG and GSEA highlight that our inv(16)/ I Tet2 i SP -/- sp AML mouse model and inv(16) AML patients share a set of functional gene expression signatures reflecting transcriptional and epigenetic rewiring, which propagates a common leukaemic phenotype. [Extracted from the article]