It has been postulated that the mutation changes the activation loop interaction with the kinase domain, although other mechanisms by which this point mutation might activate the kinase are being considered (e.g. spontaneous dimerization of the mutant Jak2), especially since other site mutations in the Jak2 kinase are also associated with/causative of myeloproliferative neoplasms. This evidence concerns the gene JAK2 and myeloproliferative neoplasm.