Indeed, certain processes we described earlier as being linked to hypertension have been observed after myocardial infarction, i.e. increased angiotensin‐II (Ang‐II) secretion (Sutton & Sharpe, 2000) and subsequent fibrosis in non‐infarcted myocardium (Volders, 1993); the hyperinnervation of non‐infarcted myocardium has also been described (Zhou et al. The gene discussed is AGT; the disease is Hypertension.