Myelofibrosis (MF) is a chronic malignancy characterised by marrow fibrosis and myeloproliferation caused by a constitutive activation of the Janus-activated kinase (JAK) transcription signalling pathway. This constitutive activation is usually the result of mutations in the driver genes JAK2, myeloproliferative leukaemia virus (MPL) or calreticulin (CALR).1 The most important clinical manifestation of MF consists of splenomegaly, in addition to hepatomegaly, cytopenia (mainly anaemia), and constitutional symptoms.2 MF significantly decreases the life expectancy of patients with a median survival of less than six years.3 During the 37th general annual meeting of the Belgian Haematology Society, professor Jean-Jacques Kiladjian (Saint Louis Hospital, Paris, France) discussed the contemporary management of this disease.