Interestingly, monoallelic patients die not differ from TP53 wildtype patients in outcomes and therapy response which would not really support a dominant-negative activity of these mutations (at least in the context of MDS).147 However, in at least 80% of TP53-mutated AML patients, more than 1 genetic alteration is present, reflecting the requirement for different oncogenic cooperation mechanisms.135 Indeed, TP53 mutations were shown to cooperate with multiple cellular signaling pathways. This evidence concerns the gene TP53 and myelodysplastic syndrome.