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. This evidence concerns the gene JAK2 and graft versus host disease.