Further in vitro and in vivo studies suggested that PIM1 can regulate the activation of the NLRP3 inflammasome by regulating intracellular Ca2+, while PIM1 inhibition suppresses NFATc1 signaling and NLRP3 inflammasome signaling in mouse and human podocytes, thus improving the clinical symptoms and pathological damage of LN (7). The gene discussed is NLRP3; the disease is lobular neoplasia.