TLR2 can form a dimer with the PI3 enzyme to increase the activity of the P-Akt signaling pathway and promote the anti-apoptotic effect of the cerebral ischemia protective agent, resulting in the cerebral ischemia protection [67], indicating that the PI3-Akt signaling pathway plays an important role in the brain protection of TLR2 ligand Pam3CSK4 and TLR9 ligand CpG-ODN postconditioning. The gene discussed is AKT1; the disease is brain ischemia.