These disorders commonly result from constitutive activation of JAK2 signalling through mutation of JAK2, frequently via the JAK2 V617F mutation (especially in polycythaemia vera), but also from JAK2 exon 12 mutations, or mutation of the TPO receptor (MPL), or mutations of LNK, a negative regulator of JAK2 [79–81]. This evidence concerns the gene JAK2 and acquired polycythemia vera.