The neuroprotective effects of caffeine involved the antagonism of the adenosine A2A receptor, down-regulating the down streaming phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway, and avoiding excessive calcium releasing-related neurotoxicity and neuroinflammation [10], which has been experimentally demonstrated in several in vivo models of PD [11,12,13,14]. The gene discussed is AKT1; the disease is Parkinson disease.