SMAD3 and asthma: Our group has recently demonstrated, utilising a dichotomous system of high versus low risk atopy/non-atopic susceptibility to asthma (BN/PVG strain rats), that co-exposure to aeroallergen (ovalbulmin) and rhinovirus infection (rodent equivalent = attenuated mengovirus), resulted in exaggerated transcriptional profiles in susceptible lungs and regulation of pathways by TGFB1/SMAD3 signal was identified in high risk animals [50].