Further validation with a model of inducible knockout rather than knockdown of IL-4Rα would shed more light on what the situation really is i.e. whether a minimal level of intact IL-4Rα signaling is sufficient to drive host protective response to secondary Nematode infection or whether hitherto unappreciated IL-4Rα-independent pathways might drive such protective Th2 memory and responses. This evidence concerns the gene IL4R and infection.