Cardiomyocyte dysfunction, increased arterial stiffness, reduced nitric oxide availability leading to endothelial dysfunction, increased insulin-like growth factor-2-mediated cardiac hypertrophy, dysfunction of the vascular smooth cells, impaired cardiac contractility, abnormal transforming growth factor-beta signalling, reduced nephron number and epigenetic alterations are the proposed pathophysiologic mechanisms linking SGA and preterm birth to increased CVD risk.94–98. The gene discussed is IGF2; the disease is endothelial dysfunction.