In fact, preconditioning positively affects the integrity of mitochondrial oxidative phosphorylation after cerebral ischemia, prevents mitochondrial swelling, protects mitochondrial energy metabolism during cerebral ischemia by avoiding ATP consumption, and increases Mn-SOD expression and activity through the NO/Ras/ERK1-2 pathway [30–33]. The gene discussed is SOD2; the disease is brain ischemia.