Since ADAP deficient CD8+ T cells reduce TGF-β1/CD103 expression and decrease the ability to protect from H5N1 virus infection, further investigation should ask whether ADAP regulates suppressive function of CD103+CD8+ T cells, whether the TGF-β1/TβRI-ADAP-TRAF6-TAK1 pathway represents a general mechanism for reciprocal TGF-β1-integrin crosstalk to mediate inflammation-associated autoimmune diseases or graft transplantation. The gene discussed is TRAF6; the disease is autoimmune disease.