Although the pathophysiologies of MS and EAE are multifactorial and complex, we set to explore the role of cathepsin Z on the NLRP3 inflammasome in the context of silicosis, starting with the hypothesis that cathepsin Z amplifies inflammation and pathology in silicosis through the enhancement of NLRP3-dependent generation of IL-1β. The gene discussed is NLRP3; the disease is silicosis.