Pre-clinical researches in atherosclerotic plaque formation, vulnerable plaque rupture, occurrence of AIS, and post-stroke recovery have confirmed that LXA4 or its analogs resolute acute inflammation and prevent chronic inflammation by activating formyl peptide receptor type 2/LXA4 receptor (FPR2/ALX) expressed on various target cells (e.g., endothelial cells, leukocytes, and microglia/macrophages). This evidence concerns the gene FPR2 and Stroke.