While current studies have delineated the core roles of ferroptosis (via the System Xc−–GSH–GPX4 axis, iron overload, lipid peroxidation, and mitochondrial dysfunction) and identified antioxidant networks (Nrf2/Sirtuins/FTH1) as therapeutic targets in DN, several critical research gaps persist that hinder a comprehensive understanding of ferroptosis-driven DN progression and translational application; addressing these gaps will significantly enhance the clinical relevance and depth of this field. The gene discussed is GPX4; the disease is liver dysplastic nodule.