TMEM16A is upregulated after ischemic stroke, and knockdown of TMEM16A in brain endothelial cells leads to attenuation of inflammation through the decrease in activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and intercellular adhesion molecule 1 (ICAM-1) [52]. This evidence concerns the gene NFKB1 and ischemic stroke.