Given the predisposition of BALB/c animals to develop type 2 responses, it is possible that genetic background strain polymorphisms (at non-WAS loci) associated with heightened type 2 immunity synergize with WASp-deficiency to precipitate overt type 2 and type17 cutaneous inflammation. This evidence concerns the gene WAS and hyperinsulinemic hypoglycemia, familial, 4.