Se can weaken the oxidative stress of activated endoplasmic reticulum and reduce apoptosis of smooth muscle cells.55 Se can reduce the infarct size and the content of TNF-α after ischemia by inhibiting the NF-κB pathway.56 However, the specific molecular mechanisms involved in the inhibition of Se on microglial activation remain unclear, and need further studies. The gene discussed is NFKB1; the disease is ischemia.