Using the LCWE mouse model, a logical progression of experiments demonstrated that (i) bone marrow-derived macrophages secrete high levels of IL-1β and TNFα; (ii) IL-1β is processed from pro-IL-1β by CASP1 through the NLRP3 inflammasome; (iii) exogenous treatment with IL-1β recreates the inflammatory phenotype in CASP1 deficient mice; and (iv) IL-1R-deficient mice or mice treated with the recombinant IL-1RA, anakinra fail to develop the arteritis lesions. This evidence concerns the gene IL1B and arteritis.