There may be plausible mechanisms by which prenatal PAH exposure could prevent or reduce airway symptoms (Rosa et al., 2011), for example by inhibiting B cell growth (Mann et al., 2001) or inducing pre-B cell apoptosis (Allan et al., 2006), which could be hypothesized to downregulate IgE production and thereby lead to a decrease in respiratory symptoms related to atopic asthma. The gene discussed is IGHE; the disease is atopic asthma.