In western blot analyses, the hepatic tissues of Atg16l1MKI mice exhibited reduced expression of p-ASK1, p-p38, and C-caspase-3 following CCl4-induced or BDL-induced HF, indicating a protective role of myeloid Atg16l1 knock-in against fibrotic signaling pathways, in contrast to the control Atg16l1ΔMφ mice (Figure 6H). The gene discussed is ATG16L1; the disease is hydrops fetalis.