In this model, inappropriate expression of protooncogenes, or down-regulation of tumor suppressors, could result in a pre-transformed state, similar to myelodysplastic syndrome, a notion corroborated by another study of aging in murine HSC [4] in which Runx1, Pml, and other protooncogenes were up-regulated with age. This evidence concerns the gene PML and myelodysplastic syndrome.