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Ferroptosis is a regulated form of cell death driven by iron-dependent lipid peroxidation, characterized by disruption of iron homeostasis, imbalance in the antioxidant system, and accumulation of lipid peroxides. Its core execution machinery is highly conserved across tissues, whereas disease-specific upstream nodes dictate pathway activation and progression in different pathological contexts. In autoimmune hepatitis (AIH), ferroptosis is governed by a "bidirectional imbalance" between enhanced pro-death signals and compromised anti-death protective mechanisms, further modulated by endocrine and metabolic factors. This imbalance collectively lowers the ferroptosis threshold in hepatocytes, amplifying their susceptibility to ferroptotic cell death. Although hepatocyte ferroptosis has been observed in experimental cholestasis models, these models do not directly represent the pathological process of primary biliary cholangitis (PBC). In PBC patients, recent studies have identified ferroptosis signals in monocyte-derived macrophages, but ferroptosis in biliary epithelial cells remains unconfirmed. In primary sclerosing cholangitis (PSC), despite elevated oxidative stress markers, the absence of core ferroptosis executioner molecules precludes any definitive link to ferroptosis. This review comprehensively summarizes the ferroptosis regulatory network and its disease-specific manifestations across autoimmune liver diseases, with a focus on AIH-specific nodes as potential precision intervention targets. We also propose a phase-based therapeutic framework and discuss safety considerations, as well as key challenges for clinical translation.