Unfortunately, in vitro and xenotransplanted models have a limited ability to reproduce the natural cancer microenvironment [35], thus, this work did not clarify how inactivation of TP53 directly increases chromosomal instability, inducing CK in MDS, nor how it allows chromosomally unstable HSC to bypass senescence or apoptosis and to survive [34]. The gene discussed is TP53; the disease is myelodysplastic syndrome.