Both populations of cells were subjected to fluorescence in situ hybridization (FISH) testing and next-generation sequencing (NGS) which revealed an abnormal clone with the deletion of the long arm of chromosome seven (7q-) and RUNX1 and NF1 among myeloid cells, suggestive of adverse risk MDS-related AML. Here, RUNX1 is linked to myelodysplastic syndrome.