IntroductionChronic inducible urticaria (CIndU) is a heterogeneous disorder characterized by the development of transient wheals or angioedema in response to specific environmental or physical stimuli[1]. Among the various subtypes, touch-induced urticaria is defined by the appearance of erythematous, pruritic wheals after minimal mechanical stimulation, such as stroking the skin, friction from clothing, or pressure from surfaces[1]. These lesions typically arise within minutes and resolve spontaneously within a few hours[1]; however, recurrent episodes can significantly impair quality of life and disrupt daily activities, particularly in young adults and students[2].Management of CIndU is challenging due to its variable response to standard therapy[3]. Non-sedating H1 antihistamines constitute the first-line treatment, with doses escalated up to fourfold in refractory cases[4]. H2 blockers or short courses of systemic corticosteroids may be added when antihistamines fail to control symptoms[1]. Despite these interventions, a subset of patients continues to experience severe disease manifestations, underscoring the need for alternative treatment strategies, including biologic therapy[1]Omalizumab, a monoclonal antibody targeting IgE, has demonstrated efficacy in chronic spontaneous urticaria (CSU) and select cases of CIndU that are refractory to antihistamines[5]. While elevated serum IgE is often considered a predictor of response, evidence suggests that some patients with normal or fluctuating IgE levels may still benefit from anti-IgE therapy[6]. This raises important questions about the pathophysiological role of IgE in CIndU and the mechanisms underlying omalizumab’s clinical effects, which may extend beyond IgE neutralization to include mast cell stabilization and modulation of autoreactive immune pathways[7].In this report, we describe a 20-year-old male with touch-induced CIndU and a history of childhood atopy, whose serum IgE levels fluctuated over time and whose disease severity remained consistently high. The case illustrates the limitations of relying solely on IgE to guide therapy and emphasizes the importance of phenotype-driven management strategies in refractory urticaria.