Since (a) we show in this current study that CSNK2B acts as a target of HIKER, playing an important role in Monge’s disease (29–31) and (b) application of selective CK2 inhibitors (32–34) decreased BFU-E colonies in a dose-dependent manner (P < 0.01), inhibition of CK2 activity is a potentially effective therapeutic strategy for treating excessive erythropoiesis in CMS subjects at high altitude. Here, CSNK2B is linked to glycogen storage disease VI.