Rather, we have addressed translational potential by designing a library of SMAs of which at least two (11a, 12b) mimic ES-62’s primary mechanism of action in downregulating MyD88 and also recapitulate many of its protective effects in mouse models of chronic inflammatory disease including asthma, arthritis and SLE (10, 32, 54). The gene discussed is MYD88; the disease is systemic lupus erythematosus.