Despite the improvement of erythema, they often fail to control facial flushing [13] through the blockage of vasodilatory neuropeptides release (e.g., acetylcholine and vasoactive intestinal peptide) and modulation of other neuropeptides thought to be involved in the pathogenesis of rosacea (e.g., vascular endothelial growth factor, P substance, and calcitonin gene-related peptide). This evidence concerns the gene TAC1 and rosacea.