After stroke, necrotic lesion produces abundant damage-associated molecular patterns (DAMPs) [47], such as mitochondrial DNA [48], ATP [49], and carboxyalkylpyrroles [50], to which injured brain cells exposed secret inflammation mediators, such as platelet-activating factor (PAF), TNF-α and IL-1β, and chemokines [51, 52]. This evidence concerns the gene IL1B and stroke disorder.