Although involved regions locate at the opposite end of the GI tract, EoE and UC both invoke Th-2-mediated pathways (24, 25) with shared pro-inflammatory cytokines (mainly interleukin-5 and interleukin-13) and shared activation of downstream Janus kinase and signal transducer and activator of transcription (JAK-STAT) pathways (mainly STAT 3 and STAT 6) (26–28). This evidence concerns the gene SOAT1 and eosinophilic esophagitis.