A multi-institution team mapped chromatin accessibility across 1,563 AML patient samples and reported 16 epigenomic subgroups with distinct regulatory wiring. Led by Kyoto University and Karolinska Institute researchers, the work used ATAC-seq plus complementary profiling including RNA-seq, DNA methylation, ChIP-seq, and single-cell multiomics. The researchers reported that chromatin-based classification was stable across single-cell ATAC-seq datasets and did not align neatly with existing mutation-led frameworks, including where decision trees built from known driver alterations failed to explain subgroup identities. Clinically, the team tied epigenomic subgroup structure to improved prognostic assessment in Swedish and Japanese cohorts and reported unexpected drug sensitivities, including MEK inhibitor responses in subgroups lacking RAS-pathway mutations and ABL inhibitor sensitivity in a RUNX1-enriched subgroup.