This difference in downstream ERK1/2 activation despite similar fetal atrial aMEK1 expression in the MEK1 Tg and our novel TAMEK/MH DTg mice correlated with the different phenotypes observed with regard to congenital ASD development, as ASD was only observed in DTg mice in which atrial ERK1/2 phosphorylation was greater than that of both ventricular tissue from the same hearts and heart tissues from non-DTg littermates,. This evidence concerns the gene MAP2K1 and atrial septal defect.