We have concerns regarding both the methodology and the conclusions drawn in the recent article by Tang et al., 1 which suggests a link between proton pump inhibitor (PPI) therapy and the development of eosinophilic esophagitis (EoE) in patients with esophageal atresia (EA). The EoE diagnostic guidelines, entitled a working group on ppi-REE (AGREE) guidelines, define EoE as symptoms of esophageal dysfunction, >15 eosinophils per high powered field (hpf), and exclusion of other potential sources of eosinophilia. 2 EA patients exhibit multiple factors that may contribute to eosinophilia, including dysmotility, poor esophageal clearance, and gastroesophageal reflux disease, necessitating a comprehensive evaluation to rule out these factors before attributing EoE solely to PPI. Previous work by Yasuda et al. 3 examining esophagitis in 310 pediatric EA patients showed that, while 15% (n = 47) met the eosinophil cutoff in the AGREE guidelines, only 2% (n = 6), were diagnosed with, exhibited behaviors of, and were treated for EoE over a 2-year follow-up period. The distinction between esophageal eosinophilia and EoE, as per the 2018 AGREE guidelines, is crucial. Transient esophageal eosinophilia in EA without changing medical therapy was also observed in the Yasuda et al. cohort. 3 Thus, without follow-up data, it's unclear if the population described truly has EoE, reflux esophagitis, or some other source of esophageal eosinophilia. Without a rigorous and clearly defined outcome, the interpretation and implications of this article need to be interpreted with caution. Finally, the term esophageal dysfunction in these patients assumes that symptoms of esophageal dysfunction are secondary to eosinophilic inflammation, and not dysmotility and narrowing inherent to EA.In addition to potential overdiagnosis of EoE, the study's design raises further concerns. The authors report that cases had significantly higher cumulative PPI dose and duration of exposure. Although they controlled for sex, prematurity, and long-gap EA