These mechanisms might be associated with an ability to restrict the activation of the NF-κB [59] and JAK1/STAT1 signal pathways, the ability to regulate endoplasmic reticulum stress (ERS) after cerebral ischemia [80], and the ability to regulate the kinase 1/2 (ERK1/2) [59], PPARγ/HO-1 pathways [24], and Akt pathways [59]. The gene discussed is NFKB1; the disease is brain ischemia.