Core Viewpoint - The study highlights that tolerance to ferroptosis enhances lipid metabolism and pathogenic type 2 immunity in allergic airway inflammation, suggesting a potential therapeutic target for asthma through the modulation of antioxidant systems [1][6]. Group 1: Key Findings - Pathogenic ILC2 in allergic airway inflammation relies on cysteine for metabolic adaptation and survival [3]. - Cysteine uptake promotes the synthesis of glutathione (GSH), which works in conjunction with the upregulation of GPX4 and TXNRD1 to enhance resistance to ferroptosis by combating lipid peroxidation and reactive oxygen species (ROS) [3]. - The adaptive changes accelerate lipid acquisition and metabolism, promoting the expansion of ILC2 and Th2 cells [3]. Group 2: Implications - The study indicates that the antioxidant and ferroptosis resistance pathways enable lipid metabolism in ILC2 and Th2 cells [4]. - GPX4 and TXNRD1 are crucial in promoting pathogenic type 2 immune responses [4]. - The redox balance system represents a targetable metabolic vulnerability in airway inflammation [4].