Asthma has long been associated with a skewing of lung immunity away from a Th1 (i.e. IFNγ producing) response to a high Th2 (i.e. IL-4/13 producing) response[30] and more recent work has demonstrated no significant induction of IFNγ in BAL cells from asthma patients experimentally challenged with rhinovirus[31]. This evidence concerns the gene IFNG and asthma.