Due to the key role of JAK1/2-STAT3 pathways on T cells activation, JAK 1/2 inhibitor ruxolitinib may reduce donor alloreactive T-cell expansion and inflammatory cytokine production, and meanwhile preserve or even promote Treg recovery post-transplantation through sparing JAK3-STAT5 pathway (Spoerl et al., 2014), explaining the mechanism of action of ruxolitinib to ameliorate cGVHD related BOS. This evidence concerns the gene JAK1 and Buschke-Ollendorff syndrome.