We could say that the treatment of GVHD has three separate purposes: reducing the activated status of B and T cells (for example, JAK1/2 inhibitors can reduce the activity of Th1, Th2, and Th17, and monoclonal antibodies (mAb) act against B and T cells), exerting a pro-inflammatory effect (reducing the secretion of IL-6, TNF-α, and IL-17—for example, infliximab and etanercept), and slowing the development of fibrosis (CSF inhibitors-1, pathways of TGF-β, PDGF, spleen tyrosine kinase (Syk), and Rho-associated kinase 2) [119]. The gene discussed is JAK1; the disease is graft versus host disease.