Tiedt et al. revealed that the mice developed an ET-like phenotype when JAK2V617F expression was lower than endogenous wild-type JAK2; the mice developed a PV-like phenotype with thrombocytosis and neutrophilic features when JAK2V617F levels were approximately equal to wild type JAK2, and higher levels of JAK2V617F caused a PV-like phenotype but no platelet formation [6]. Here, JAK2 is linked to thrombocytosis disease.