Unlike the previous data, the current in vivo findings showed that the role of LPA1 in cerebral ischemia was linked to MAPK and PI3K/Akt because suppressing LPA1 activity in the ischemic brain decreased the phosphorylation of ERK1/2, p38, and JNK whereas it increased Akt phosphorylation. The gene discussed is LPAR1; the disease is brain ischemia.