SNCA and Parkinson disease: Similarly, in Parkinson’s disease, risk variants in SNCA (α-synuclein) and LRRK2 contribute to disease risk, but their pathogenic impact is mediated by post-translational modifications such as phosphorylation and ubiquitination, which influence α-synuclein aggregation and mitochondrial dysfunction.59 An optimal framework for identifying true molecular drivers of complex diseases must integrate genetic, epigenetic, transcriptomic, and proteomic data, allowing for the detection of both individual and interaction genetic elements that causally influence disease susceptibility.