Altogether, our findings are consistent with the existence of early causes of inflammation in subsets of MPN patients, which result in chronic overstimulation of myelopoiesis via the JAK2/STAT5 pathway and thus, facilitate the acquisition of JAK2 or CALR mutations that further activate JAK2/STAT5 (Figure 8). The gene discussed is CALR; the disease is myeloproliferative neoplasm.