Impaired erythropoiesis in MDS carrying a deletion on 5q has been linked to activation of TP53 upon inactivation of the ribosomal protein small subunits (RPS)-14 or -19.135 More recently, activation of TP53 during ribosomal biogenesis have been proposed to regulated normal erythroid differentiation.136 Most TP53 alterations identified in AEL and other AML subtypes are missense mutations in the DNA binding domain but their functional consequences (ie, inactivating, gain-of-function or dominant negative) remain a matter of debate. The gene discussed is TP53; the disease is myelodysplastic syndrome.