A recent study reported that hypereosinophilic syndrome, a rare adverse event of anti-cytokine treatment in RA, was resolved after JAK inhibitor.[11] Similarly, GM-CSF was reportedly involved in the pathogenesis of RA, and[8] serum eosinophils by GM-CSF have also been associated with phosphorylation of JAK 2.[12] These results suggest that induced GM-CSF expression was a common pathological factor between RA and eosinophilic diseases. The gene discussed is CSF2; the disease is rheumatoid arthritis.