Notably, in an A53T α-synuclein transgenic mouse, a familial Parkinson’s disease model, Wu et al. demonstrated that increased GRK6 and CK2α S-nitrosylation was age-dependent and associated with an increased level of p-Ser129 α-synuclein, which suggests GRK6 and CK2α S-nitrosylation as a potential therapeutic target of α-synucleinopathy. The gene discussed is SNCA; the disease is synucleinopathy.