Our analysis unveiled that ATP7B overexpression activated multiple pathways, including autoimmune thyroid disease, the intestinal immune network for IgA production, asthma, rejection of allografts, systemic lupus erythematosus, hematopoietic cell lineage, type I diabetes mellitus, leishmania infection, graft versus host disease, antigen processing and presentation, primary immunodeficiency and Nod receptor signaling pathway (Figure 6D). This evidence concerns the gene ATP7B and graft versus host disease.