药物性肝损伤（DILI）是临床用药中最常见的不良反应之一，通常由药物或草药化合物引起。与其他人群相比，癌症患者更容易因原发性或继发性肝脏恶性肿瘤、放射性肝损伤等原因出现肝功能异常，使得抗癌药物引起的肝损伤潜在不良反应在临床治疗过程中尤其值得关注。近年来，表皮生长因子受体酪氨酸激酶抑制剂（EGFR-TKIs）的应用改变了一系列实体恶性肿瘤的治疗现状。不幸的是，肝毒性发生率的增加限制了EGFR-TKIs的临床应用。 EGFR-TKIs引起肝损伤的机制很复杂。尽管经过十几年的研究，除了抑制细胞DNA合成而直接损害肝细胞导致肝细胞坏死外，其余具体机制仍不清楚，也缺乏有效的解决方案。本文重点介绍EGFR-TKI肝毒性机制的临床特点、发生率和最新进展，以及EGFR-TKI肝毒性的再激发和治疗策略。

Drug-induced liver injury (DILI) is one of the most frequently adverse reactions in clinical drug use, usually caused by drugs or herbal compounds. Compared with other populations, cancer patients are more prone to abnormal liver function due to primary or secondary liver malignant tumor, radiation-induced liver injury and other reasons, making potential adverse reactions from liver damage caused by anticancer drugs of particular concernduring clinical treatment process. In recent years, the application of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) has changed the treatment status of a series of solid malignant tumors. Unfortunately, the increasing incidence of hepatotoxicitylimits the clinical application of EGFR-TKIs. The mechanisms of liver injury caused by EGFR-TKIs were complex. Despite more than a decade of research, other than direct damage to hepatocytes caused by inhibition of cellular DNA synthesis and resulting in hepatocyte necrosis, the rest of the specific mechanisms remain unclear, and few effective solutions are available. This review focuses on the clinical feature, incidence rates and the recent advances on the discovery of mechanism of hepatotoxicity in EGFR-TKIs, as well as rechallenge and therapeutic strategies underlying hepatotoxicity of EGFR-TKIs.