In central nervous system (CNS), donor neurons overloaded with α-synuclein aggregates were recently reported as a mechanism of hijacking TNT-mediated intercellular trafficking to the neighbor cells which may contribute to the neuropathology—Parkinson's disease.10 Interestingly, the expression of mutant huntingtin (Htt) which increased the number of TNTs provided an efficient mechanism of transfer between neuronal cells to further illustrate the pathogenesis of Huntington's disease (HD).11 This evidence concerns the gene HTT and Huntington disease.