While MC903‐induced ILC2 function could be targeted by anti‐IL‐18,68 we show that chronic inflammation is independent of IL‐18, further corroborating the observed redundancy of ILC2.69, 70 Although ILC2 may contribute to genesis of acute skin inflammation, their increase in numbers under chronic inflammatory conditions is probably a consequence of an overall increase in infiltrating immune cell populations. This evidence concerns the gene IL18 and dermatitis.