This is suggestive of a maintained TH2 memory cell recall from systemic OVA sensitization which is IL‐4/IL‐13 independent.53, 54, 55, 56 This is in contrast to a similar temporal deletion of IL‐4Rα signaling prior to secondary infection with Nippostrongylus brasiliensis showing a recall role in driving type‐2 immune responses and clearance of the parasites.33 In this helminth infection model, IL‐4Rα signaling is vital in not only initiating, but also maintaining a functional TH2‐driven pathology and its associated cytokines. Here, IL4 is linked to infection.