Alternatively, mRNA- and protein-based platforms might also be suitable to deliver TRIM11, which may display a non-inferior effect with more safety.2 More interestingly, another study performed by the same group reported that TRIM11 could inhibit and reverse the formation of α-Syn fibrillar aggregates, subsequently mitigating neurodegeneration and motor defects in a mouse model of Parkinson’s disease.3 These results suggest that TRIM11 might be a powerful weapon to treat neurodegenerative diseases in a broader range. This evidence concerns the gene TRIM11 and Parkinson disease.