NLRP3 and lobular neoplasia: In conclusion, treatment with M1 dramatically improved the ASLN mice by inhibiting NLRP3 inflammasome activation in combination with autophagy induction and differentially regulating T cell functions, and the results support M1 as a new therapeutic candidate for LN patients with a status of abrupt transformation of lower-grade (mild mesangial) to higher-grade (diffuse proliferative) nephritis.