Recent preclinical studies in mouse models have revealed that baricitinib, a more specific JAK1/2 inhibitor, is superior to ruxolitinib in preventing GVHD for at least two reasons: (1) By preserving JAK3-STAT5 signaling, baricitinib is associated with increases in regulatory T cells (Tregs) that suppress GVHD (11), whereas ruxolitinib inhibits JAK3 and Tyk2.9 thus causing other adverse effects; and (2) Baricitinib has a higher half maximal inhibitory concentration (IC50) than ruxolitinib for JAK2, thus JAK2 is not overwhelmingly inhibited by baricitinib compared with ruxolitinib. Here, JAK3 is linked to graft versus host disease.