To date, several hypotheses for mechanism regarding how a single mutation can be contributed to different MPN subtypes are under investigation such as differences in the targeted hematopoietic stem cells, host modifier polymorphisms, intensity of JAK2 V617F signaling, presence of other somatic mutations, or the presence of a pre-JAK2 event that may vary according to the MPN phenotype [8]. This evidence concerns the gene JAK2 and myeloproliferative disorder.