Key to understanding the control of susceptibility to autoimmune myocarditis was the finding that adding bacterial lipopolysaccharide (LPS), interleukin (IL)-1β, or tumor necrosis factor (TNF)-α during the innate response to CB3 infection results in the development of the chronic phase of disease in resistant strains of mice (28,29). The gene discussed is IL1B; the disease is autoimmune myocarditis.