● ● ● MYELOID NEOPLASIA Comment on Zheng et al, page 156

Activatingmutations in JAK2, a tyrosine kinase that serves as a critical signaling protein for multiple cytokines, are associated withBCR-ABL1–negativemyelo-proliferative neoplasms. In this issue ofBlood, Zheng and colleagues report that the constitutively activated kinase CK2 binds to JAK2 and is required for JAK-Stat signaling, suggesting that CK2 inhibitors may provide a second, complimentary therapeutic for diseases with elevated JAK2 signaling, such asmyeloproliferative neoplasms.1 JAK family tyrosine kinases (JAK1, JAK2,JAK3, Tyk2) bind to cytokine receptors and are activated on cytokine binding. The activated JAKs phosphorylate tyrosines in themselves and in the associated cytokine re-ceptors. The resulting phosphotyrosines form binding sites for multiple signaling proteins, including the Stat transcription factors that mediate many of the actions of the activatin