CD80 and autoimmune disease: Interestingly, a CTLA‐4 splicing variant lacking the B7 binding domain was still able to control T cell activation, and expression of a B7‐nonbinding CTLA‐4 mutant in CTLA‐4 knockout T cells inhibited T cell proliferation and cytokine production.[9] In our previous study, we reported that intracellular delivery of the cytoplasmic domain of CTLA‐4 (ctCTLA‐4) in vivo ameliorated allergic inflammation, autoimmune disease, and graft rejection.[10]