This reflects the situation in the clinical presentation of MPN where p53 mutations are rarely seen at presentation but disruption in the p53 network or actual mutations in p53 are found in >50% MPN secondary leukaemias.42 It has been reported that JAK2V617F inhibits the stabilisation of p53 after induction of DNA damage via increases in MDM2 translation such that p53 has been suggested to play a role in disease progression25 and offer a valid target in MPN. Here, TP53 is linked to myeloproliferative neoplasm.