TNF-α has been implicated in the pathophysiology of GVHD at several steps in the process, including induction of apoptosis in target tissues through the TNF-α receptor; activation of macrophages, neutrophils, eosinophils, B cells, and T cells; stimulating production of additional inflammatory cytokines (IL-1, IL-6, IL-10, IL-12, and TNF-α itself); increased expression of HLA; and the facilitation of T-lymphocyte lysis. This evidence concerns the gene TNF and graft versus host disease.