EOS deficiency in spleens from Rorafl/flIl7rCre/+ mice with or without AAA suggests a congenital deficiency of IL5 in the bone‐marrow where IL5 controls EOS maturation.[38] Mice without AAA displayed significant reduction of IL5 expression by immunoblot analysis in the bone‐marrow from Rorafl/flIl7rCre/+ mice (Figure S9A, Supporting Information). This evidence concerns the gene IL5 and triple-A syndrome.