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Autoimmune hepatitis (AIH) is an enigmatic, chronic and progressive inflammatory disease of the liver that carries a high mortality rate if left untreated. Although its pathogenesis is incompletely understood, susceptibility has been linked to a combination of genetic and environmental factors. One histological hallmark of AIH is the dense infiltration of lymphocytes, macrophages and plasma cells in the liver, leading to hepatocyte damage at the periphery of the lobule and erosion of the limiting plate, a feature known as interface hepatitis.1 While hepatocyte loss is widely recognised as a key feature of AIH, the mechanisms regulating hepatocyte cell death in AIH remain poorly defined.2 Recent work has implicated ferroptosis, an iron-dependent and lipid peroxidation–driven form of regulated cell death, as an underappreciated contributor in experimental AIH.3 First described in 2012, ferroptosis is mechanistically and morphologically distinct from apoptosis or necroptosis. It is defined by iron accumulation, reactive oxygen species (ROS) overload and peroxidation of polyunsaturated phospholipids, along with the characteristic appearance of shrunken, electron-dense mitochondria and inactivation of the glutathione (GSH)/glutathione peroxidase 4 (GPX4) detoxification system.4 Ferroptosis is controlled by a complex interplay between pro-death metabolic signals (eg, iron, arachidonic acid, PUFAs) and anti-ferroptotic defence systems, including the cystine-GSH-GPX4 axis, the FSP1 coenzyme Q10 - ferroptosis suppressor Protein 1 (CoQ10-FSP1) pathway and the GCH1-BH4 system. Cytokines such as interferon-γ (IFN-γ) can promote ferroptosis by downregulating SLC7A11 or enhancing lipid peroxidation.5 In this context, the cytoplasmic protein A20, also known as tumour necrosis factor alpha-induced protein 3 (TNFAIP3), emerges as a compelling regulatory nodal point. A20 is a pleiotropically expressed cytoplasmic protein and it is best known as a ubiquitin-editing enzyme that restricts nuclear factor kappa b subunit 1 (NF-κB)-driven inflammation and preserves cell survival. A20 serves as a critical upstream regulator and has been implicated in diverse inflammatory and autoimmune diseases, underscoring its importance in maintaining tissue homeostasis.6