In contrast, in neurodegenerative paradigms (e.g., toxin-based Parkinson's disease models and ischemia-reperfusion injury), eEF1A2 is primarily implicated as a contributory node within oxidative stress, autophagy/mitophagy, and inflammatory signaling pathways, largely based on cellular and animal model evidence rather than Mendelian causality. This evidence concerns the gene EEF1A2 and Parkinson disease.