Chronic spontaneous urticaria (CSU) creates substantial patient burden through persistent wheals, angioedema, and debilitating itch that severely disrupts daily functioning. Emerging evidence positions type 2 inflammation as a driver of CSU pathogenesis. IL-4 plays a particularly crucial role by stimulating excessive IgE production and promoting formation of IgG anti-IgE autoantibodies—both pathways that trigger mast cell degranulation and subsequent CSU symptoms. This mechanistic understanding has opened therapeutic opportunities targeting type 2 inflammatory pathways for patients who remain symptomatic despite standard antihistamine therapy.