Stephenson et al. present results of their investigation into mechanisms of acetaminophen sensitivity risk in children with moderate to severe asthma in a Letter to the Editor in this issue (J Allergy Clin Immunol 2012;129:863-865.e2). Based on their previous findings of (nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor-associated glutathione deficiency in children with severe asthma, the authors report decreased expression of the aryl hydrocarbon receptor (AHR) and AHR nuclear translocator heterodimer genes (ARNT), which regulates toxin metabolism, after ex vivo acetaminophen exposure. Phase II toxin metabolism enzymes, such as dehydrogenases, hydrolases, and kinases were decreased in children with asthma compared to controls. Extracellular glutathione release was unaltered in children with asthma, whereas glutathione was elevated in controls after acetaminophen exposure. Stephenson et al. note that AHR/ARNT regulates Nrf2 signaling, which is consistent with their previous research results.