[5][6] The distinguishing feature between janus kinase 2 and other JAK kinases is the lack of Src homology binding domains (SH2/SH3) and the presence of up to seven JAK homology domains (JH1-JH7).

[9] JAK2 orthologs[10] have been identified in all mammals for which complete genome data are available.

[11][12][13] Mutations in JAK2 have been implicated in polycythemia vera, essential thrombocythemia, and myelofibrosis as well as other myeloproliferative disorders.

[14] This mutation (V617F), a change of valine to phenylalanine at the 617 position, appears to render hematopoietic cells more sensitive to growth factors such as erythropoietin and thrombopoietin, because the receptors for these growth factors require JAK2 for signal transduction.

[15] Janus kinase 2 has been shown to interact with: Prolactin signals through JAK2 are dependent on STAT5, and on the RUSH transcription factors.