In this study, we just focused on CK2α and GRK6 because studies have shown that they are the primarily kinases that phosphorylate α-syn at S129 [21, 27–29] Taken together, the mouse PD model suggested that even heterogenic deletion of nNOS could have a significant effect on the metabolism of α-syn and pSer129 α-syn level in an age-dependent manner. Here, GRK6 is linked to Parkinson disease.