CK2 increases JAK2 activity and signaling. As reported by Zheng and colleagues, the binding of active CK2 to JAK2 appears to be essential for oncostatin M (OSM)–dependent activation of JAK2 and signaling molecules downstream of JAK2, including Stats, ERKs, and expression of target genes including the gene for suppressor of cytokine signaling-3 (SOCS-3).¹  HEL cells and cells from patients with PV express the hyperactive JAK2 V617F. In these cells, the binding of CK2 to JAK2 V617F is essential for maximal JAK2 activity and the expression of the antiapoptotic protein Bcl-xL. Inhibition of CK2 activity results in a substantial decrease in JAK2, Stat3, and ERK activity, decreased Bcl-xL, and increased apoptosis.