Allergic responses are defined by hypersensitive reactions against foreign antigens that activate immune cell interactions, leading B lymphocytes to produce IgE. This results in tissue mast cells and circulating basophil cells releasing leukotrienes and histamine, which causes an early inflammatory response; in the late phase, immune cells release chemokines and cytokines. Ferroptosis is an iron-dependently regulated cell death process in which excessive production of reactive oxygen species (ROS) causes massive lipid peroxidation–mediated membrane damage. Allergens, IgE regulation, inflammatory cytokines, and lipid metabolism from an allergic response can induce ferroptosis, which can then enhance the allergic response. This review summarizes the mechanism of ferroptosis and its key regulators. We particularly focus on the potential roles of allergen triggers, IgE regulation, inflammatory cytokines, and lipid metabolism in ferroptosis. We also describe recent research progress regarding ferroptosis in allergic asthma, allergic rhinitis, and allergic dermatitis. Further research on the process of ferroptosis in allergic responses and diseases can aid potential novel therapeutic tools.