Several studies were done to investigate molecular mechanisms of how oxidative stress influenced renal injury and stroke; in the kidney, oxidative stress (mostly generated in renal mesangial cells) was shown to activate the protein kinase C (PKC) and the mitogen-activated protein kinases (MAPK), which then promoted the translocation of transcription factors such as NF-κB and AP-1 into the nucleus that eventually facilitated expression of the gene of extra cellular matrix proteins [26]. This evidence concerns the gene PRRT2 and stroke disorder.