<p>Liver cancer, including hepatocellular carcinoma (HCC) and hepatoblastoma (HB), remains a major global health burden with limited therapeutic options and poor outcomes in advanced disease. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a critical tumor-suppressive mechanism; however, adaptive resistance to ferroptosis represents a major barrier to effective therapy. Recent studies identify RNA methylation, particularly <i>N</i>⁶-methyladenosine (m⁶A) and 5-methylcytidine (m⁵C), as a key epitranscriptomic layer that dynamically regulates ferroptosis sensitivity. Rather than acting on isolated targets, RNA methylation reprograms ferroptosis through coordinated control of antioxidant defense, lipid metabolism, autophagy, and stress adaptation pathways. This review synthesizes current evidence on how m⁶A- and m⁵C-mediated regulation shapes ferroptosis in liver cancer, highlighting context-dependent effects across tumor types, microenvironmental conditions, and therapeutic settings. Importantly, we propose that RNA methylation functions as a context-dependent molecular switch that integrates metabolic state and treatment pressure to determine ferroptotic vulnerability. From a translational perspective, these insights support the development of biomarker-guided stratification strategies and combination therapies targeting epitranscriptomic regulation to overcome ferroptosis resistance. Overall, understanding the RNA methylation–ferroptosis axis may provide a conceptual framework for precision therapeutic intervention in liver cancer.</p>