SHRs are widely used as an animal model to study the pathophysiology and management of hypertension, and a range of abnormalities have been reported in SHRs relative to the normal counterparts, including defection in both Akt-dependent and Akt-independent signaling pathways (Iaccarino et al., 2004; Hsiao et al., 2008), an increased vasoactive intestinal peptide-mRNA expression (Avidor et al., 1989), and a reduced content of vasopressin in the brain (Lang et al., 1981), among others, which are supposed to be either a causal or a compensatory factor for the hypertension on SHRs. The gene discussed is AKT1; the disease is hypertensive disorder.