P53 is particularly important in patients with MDS harboring an interstitial deletion of chromosome 5q [del(5q)], where RPS14 haploinsufficiency results in ribosomal stress liberating free ribosomal proteins that bind to, and trigger degradation of the primary negative regulator of p53, the human homologue of murine double minute-2 (MDM2) [2–4]. Here, TP53 is linked to myelodysplastic syndrome.