Analysis of hepatic mRNA expression levels of pro-inflammatory cytokines in conjunction with the anti-inflammatory cytokine in Atg16l1ΔMφ mice with HF induced by CCl4 (Figure 4B) or BDL (Figure 4C) revealed a pronounced enhancement in the activation of hepatic inflammatory signaling pathways relative to the Atg16l1FL/FL mice, indicative of a more robust inflammatory response in the context of macrophage Atg16l1 deficiency during HF. The gene discussed is ATG16L1; the disease is hydrops fetalis.