However, in autoimmune diseases, the superior affinity of CTLA4 for its ligands led to the use of a CTLA4-immunoglobulin fusion protein (CTLA4-Ig) as an inhibitor of immune responses in vivo; the rationale being that it would bind to CD80 and CD86 and block their interaction with CD28 [26, 27]. The gene discussed is CD86; the disease is autoimmune disease.