The PD-associated A53T and A30P mutations in α-synuclein shift the native tetrameric conformation towards the monomeric conformation [32], suggesting that the destabilization of the α-helical tetramers and the increased number of unfolded monomers facilitate the aggregation-mediated pathology of α-synuclein in PD. The gene discussed is SNCA; the disease is Parkinson disease.