This is exemplified by the fact that liposomes loaded with NFkB inhibitors targeting APC in situ, suppress the cellular responsiveness to NF-kB and induce antigen-specific FoxP3+ regulatory T cells in an animal model of arthritis (79) and that administration of phosphatidylserine-rich liposomes loaded with disease-specific autoantigens lead to a beneficial effect in experimental models of T1D and MS (80, 81). The gene discussed is NFKB1; the disease is type 1 diabetes mellitus.