Mice deficient in IL-1β, IL-1R or MyD88, but not IL-1α, exhibit a severe impairment in neutrophil abscess formation at the site of infection in this mouse model of S. aureus intradermal infection [3], [11], indicating that IL-1β is the major cytokine that initiates the IL-1R/MyD88-dependent pathway for neutrophil recruitment. The gene discussed is IL1A; the disease is abscess.