Notably, despite the convergent mechanistic pathways of MPN-driver mutations, it appears that the ability of IFNα to deplete the MPN stem cell clone is largely restricted to patients with JAK2V617F mutations, and that CALR mutant MPN is less likely to achieve molecular remissions in response to pegylated IFNα therapy, despite achieving similar outcomes in terms of haematological responses12,13. Here, IFNA1 is linked to myeloproliferative disorder.