AGT and transposition of the great arteries: In light of a recent pathophysiological hypothesis for TGA postulating a role for the renin–angiotensin system, specifically Angiotensin II (AT-II) and interactions of central AT-II type 1 and N-methyl-d-aspartate receptors [1] it bears mentioning that plasma levels of AT-II peak mid-morning [51], which coincides with the major peak of TGA occurrence.