Children who were clinically reactive to peanut (including those with anaphylaxis) had higher specific IgE levels to Ara h 1, Ara h 2, and Ara h 3 than asymptomatic peanut-sensitized children did (p < 0.00001). Elevated specific IgE to Ara h 2 was the major contributor to accurate discrimination between clinical reactivity to peanut and asymptomatic sensitization to peanut (99.1% sensitivity, 98.3% specificity, and 1.2% misclassification rate) and had a higher discriminative accuracy than IgE to whole peanut extract (p = 0.008) [22].