PLEKHN1 and Platelet storage pool disease: Therefore, we suggest that the alteration of rs28499371 polymorphism in the PLEKHN1 gene might play some pathophysiological roles in the pathogenesis of sPD through affecting the production of nerve myelin sheath, the destabilization of 3′-UTR-mediated mRNA, the regulation of neural cell apoptosis, and the response of hypoxia, subsequently contributing to nerve myelin sheath deletion, excessive neural cell apoptosis, and increased ROS production, which ultimately result in the death of the DA neuron in sPD.