As IL-10–dependent M2 macrophage polarization is mediated through JAK-STAT signaling, and inhibition of M2 macrophage polarization was demonstrated by an in vitro study showing that ruxolitinib inhibited Th2-associated cytokines-induced M2 macrophage polarization [6], the use of ruxolitinib might have potential as a new treatment for AITL. The gene discussed is SOAT1; the disease is angioimmunoblastic T-cell lymphoma.