It results in the release of oxidative stress products and inflammatory cytokines/chemokines (IL1, IL6, IL15, CCL2, CXCL1, CXCL10, CXCL12, and IP-10), proinflammatory associated small molecules [S100 Ca2+-binding protein B (S100B) and nitric oxide (NO)] that enhance the inflammatory post-stroke response (Yamashita et al., 2000; Hill et al., 2004; Mori et al., 2008; Shin et al., 2014; Liu H. et al., 2015; Chen et al., 2018). This evidence concerns the gene IL1B and stroke disorder.