To the Editor: Chronic spontaneous urticaria (CSU) presents as recurrent itchy wheals, angioedema, or both for at least 6 weeks without a specific trigger.1 Roughly half of the patients with CSU achieve symptomatic control with H1-antihistamine therapy at approved doses, increased doses, or with additional therapies such as leukotriene receptor antagonists.1 CSU can be unpredictable and debilitating for patients because of a lack of clinical response.2 Recently, omalizumab, a neutralizing anti-IgE mAb, has gained approval for treatment of patients with CSU on the basis of evidence of substantial efficacy.3 However, the treatment benefit with omalizumab is usually lost when treatment is stopped. Specific IgE may target an endogenous antigen, a hypothesis supported by evidence that approximately 50% of patients with CSU have elevated levels of antithyroperoxidase IgE.5 Quilizumab, a humanized, afucosylated, monoclonal IgG1 antibody, binds membrane IgE at the M1-prime segment, which is absent in soluble IgE.6 In animal studies, quilizumab bound membrane IgE on IgE-switched B cells and plasmablasts and depleted them through apoptosis and antibody-dependent cell-mediated cytotoxicity.6 In clinical trials, quilizumab reduced serum total and specific IgE levels in healthy volunteers and in patients with allergic rhinitis or mild asthma.7,8 These reductions were sustained for at least 6 months after the last dose, suggesting that quilizumab affected long-term IgE memory.