JAK2 and myeloproliferative neoplasm: The most frequently occurring gain-of-function JAK2 mutation, V617F, gives rise to a constitutively active JAK2 kinase, which drives the JAK/STAT signaling that leads to excessive proliferation and survival of myeloid progenitor cells in most of the Philadelphia chromosome-negative classical myeloproliferative neoplasms (MPNs) [2].