In light of previous findings that Tet showed high affinity binding to alveolar macrophages and strongly inhibited production of IL-1β in macrophages [29, 30], we thus speculated that the attenuation of silicosis by Tet might be ascribed to upstream blockade or inhibition of IL-1β and/or NLRP3 inflammasome. The gene discussed is NLRP3; the disease is silicosis.