It is therefore highly plausible that some TET2/ASXL1 co-mutated cases evolved from long-standing, undiagnosed low-blast-count MDS or clonal hematopoiesis of indeterminate potential (CHIP) that rapidly progressed to overt AML before the MDS phase became clinically detectable. This evidence concerns the gene ASXL1 and myelodysplastic syndrome.