TAC1 and atrial fibrillation: In these models, one might block the activity of substance P by specific receptor antagonists, or one might use tachykinin 1-deficient (Tac1−/−) mice (no SP) in order to specify the role of substance P. In the rat model, Watson et al. described that transforming growth factor beta is an outstandingly important stimulus of AF, which nicely fits to the fact that substance P is a perfect stimulator of this cytokine [40].