Researchers first proposed in 2008 that after incubating mouse primary MG with Aβ, NLRP3 inflammasome was activated, and the phagocytosis of fibrotic Aβ by MG can cause the swelling and rupture of lysosomes and release cathepsin B, and promote the mature release of IL-1β, TNF-α and other inflammatory factors and the production of chemokines; the initiation of NLRP3 inflammasome in MG also depends on the activation of IL-1β and caspase-1 (Halle et al., 2008; Salminen et al., 2008). The gene discussed is IL1B; the disease is myasthenia gravis.