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Emerging clonal complexity has brought into question the way in which we perceive and, in turn, treat disorders of the hematopoietic system. Former models of cell-intrinsic clonal dominance driven by acquisition of driver genes in a stereotypic sequence are often insufficient in explaining observations such as clonal hematopoiesis, and new paradigms are in order. Here, we review the evidence both within the hematologic malignancy field and also borrow from perspectives rooted in evolutionarydoi:10.1158/2643-3230.bcd-20-0219 pmid:34027415 pmcid:PMC8133502 fatcat:azo3n3zpzffpdguj737xhosshy