Research findings have indicated that, in comparison to cells in a homeostatic state, upregulated proteoglycans binding to CD14/CD44 activate TLR2/4 in damaged cells [7]; During metabolic disorders, the accumulation of fatty acids activates the NLRP3 inflammasome via the PERK/eIF2αpathway [8]; While potassium ion efflux [9, 10] or CLIC-mediated Cl- efflux triggers NLRP3 assembly [11]. This evidence concerns the gene NLRP3 and metabolic disease.