JAK2 and myeloproliferative neoplasm: However, the description of other recurrent mutations, the evidence that MPN patients can respond to JAK2 inhibitors regardless of JAK2 mutation status, and the knowledge that many receptors and substrates may lead to the activation of the JAK/STAT, MAPK and PI3K/AKT/mTOR pathways through mechanisms other than the JAK2 pathway suggest that other interacting proteins may be involved in the pathophysiology of these diseases [4, 5].