Additional evidence suggests that NLRP3 inflammasome blockade therapy using IP-Se-06 (selenylated imidazo[1,2-a]pyridine) induces anti-proliferation of glioma cells via inhibition of p38 MAPK and p-p38, leading to inhibition of the NLRP3 inflammasome [129]. In addition, in-depth glioma studies were conducted on the effects and mechanisms of the NLRP3 inflammasome in terms of cellular plasticity including M1 macrophage polarization and drug resistance [130, 131]. Here, NLRP3 is linked to central nervous system cancer.