RIP1 kinase enhances the progress of NASH, by activating NLRP3 inflammasome in liver macrophages (hematopoietic-derived macrophages).[33] HBeAg can inhibit the activation of NLPR3 in KCs to promote the HBV persistence and immune tolerance.[34] Activation of NLRP3 in KCs contributes to liver fibrosis in schistosomiasis infection through via NF-κB.[35]. This evidence concerns the gene NLRP3 and metabolic dysfunction-associated steatohepatitis.