This approach is clearly validated (construct validity, Fig. 2) in patients, by (i) the presence of alpha-synuclein accumulation in Lewy bodies [27], a pathological hallmark of synucleinopathies, by (ii) the fact that multiplication of SNCA causes familial forms of PD, and by (iii) the observation that polymorphisms in non-coding regions of SNCA increase PD risk or progression [28–30]. Here, SNCA is linked to Parkinson disease.