In addition, an experimental model of 70% PH in mice with genetically inbred resistance to CCl4-induced fibrosis (through A/J allele of Nlrc4, which modulates the resolution of hepatic fibrosis), found that the NLR family NLRC4 inflammasome-driven production of inflammatory cytokine signaling (TNF-α, IL-1β, and IL-18) led to benefits on damage and hepatocyte proliferation [143]. Here, NLRC4 is linked to fibrosis.