Since treatment of JAK2-mutant MPN patients with ruxolitinib, a JAK1/2 inhibitor that inhibits STAT1 tyrosine phosphorylation, does not induce differentiation, a combination of CA and ruxolitinib has been proposed as a strategy to treat JAK2-mutant MPNs characterized by STAT1 hyperphosphorylation [147]. This evidence concerns the gene JAK2 and myeloproliferative neoplasm.