While this genetic data alone suggests JAK2 activation plays an etiologic role in MPNs, a plethora of mouse models have demonstrated that expression of JAK2-V617F, as well as other JAK2-activating mutations found in MPNs, can generate human MPN-like phenotypes in mice [8, 9, 12–19]. The gene discussed is JAK2; the disease is myeloproliferative disorder.