Together with the changing prevalence of VIP-positive cholinergic stellate neurons in humans, from neonates and children to adults (Roudenok et al. 1999), and the increased expression of VIP in sympathetic neurons after acute myocardial infarction (Roudenok and Schmitt 2001), questions regarding the stability and plasticity of transmitter phenotypes during aging and disease processes represent key issues that must be addressed. The gene discussed is VIP; the disease is acute myocardial infarction.