TMX treatment decreases the neuronal apoptosis and cerebral infarction volumes by reducing interleukin-1B (IL-1B) production and increasing the neuronal phosphorylated extracellular signal-regulated kinases 1 and 2 (p-ERK1/2) and B-cell lymphoma 2 (Bcl2) expressions [227]. This evidence concerns the gene MAPK3 and cerebral infarction.