In a transient model of focal cerebral ischemia, apelin-13 reduces brain injuries and postischemic cerebral edema in a dose-dependent manner, likely through inhibiting neuronal apoptosis, which may be mediated by many mechanisms, such as activating AMPK, PI3K/AKT, and ERK1/2 signaling pathways (47, 49, 50, 103). The gene discussed is AKT1; the disease is edema.