In 2008, alpha-gal syndrome (AGS) was described as an IgE-mediated food allergy toward the oligosaccharide galactose-α-1,3-galactose (alpha-gal) present in nonprimate mammals and New World monkeys.1 AGS is characterized by urticaria, angioedema, pruritus, gastrointestinal symptoms, and/or anaphylaxis developing 2 to 6 hours after consumption of mammalian meat or other alpha-gal–containing products. The diagnosis of AGS is usually made on the basis of these delayed symptoms and elevated level of serum-specific IgE to alpha-gal. The recognition of AGS started with a distinct geographic pattern of patients experiencing anaphylaxis after their first infusion with cetuximab, a novel mAb for treating cancer.1 It was shown that the anaphylactic episodes occurred in patients with preexisting antibodies to alpha-gal in geographic areas with a high prevalence of ticks.1 A strong link between tick bites and subsequent AGS has been established, and it has been indicated that levels of IgE to alpha-gal seem to decrease if the patient avoids new tick bites and, accordingly, that a new tick bite can yield a marked increase in the alpha-gal IgE level.2,3 Further, 2 recent case reports of AGS described urticaria at the site of a previous tick bite, which was labeled as recall urticaria.4,5 In particular, recall urticaria has been described in case reports in relation to allergen-specific immunotherapy with a local reaction at the site of previous allergen injections after, for example, administration of a new allergen6 or environmental exposure to the allergen,7 drugs,8 or food.9 In this case, we have more than 10 years of repeated measurements of levels of IgE to alpha-gal, showing the first longitudinal data on how IgE level changes over the course of a decade. Additionally, this case highlights the potential importance of symptoms related to the tick bite.