Modeling the most commonly detected ASXL1 mutation using Asxl1G643fs/+ mice (heterozygous knock-in of Asxl1 mutant G643WfsX12 mimicking ASXL1G646fs) demonstrated abnormal hematopoiesis and recapitulated human low-risk MDS with some mice developing MDS/MPN-like disease after a long latency. This evidence concerns the gene ASXL1 and myelodysplastic syndrome.