This proposal, like the age-associated risk proposal described above, was based on phenotype not genotype, and we now recognize that disease behavior in MPNs is genetically-based, and in part driven by the MPN driver MAB, the important role of which, particularly with regard to JAK2 mutations, dictates clinical behavior in PV [78] and PMF [79]. The gene discussed is JAK2; the disease is myeloproliferative disorder.