Indeed, although HDAC6‐mediated HSP90 acetylation level was thought to mediate JAK2 stability and activity, a recent report identified HDAC11 as the main target to control the JAK–STAT pathway, cell survival and proliferation in leukaemic cells carrying the JAK2V617F mutation and in MPN induced in mice by the MPLW515L mutation.53 This evidence concerns the gene HDAC11 and myeloproliferative disorder.