Thus, a prudent approach would take the data reported by Watts et al. [92] either as an acceleration, or—if the absence of protein aggregation and clinical disease were shown to persist in M83+/−: Gfap-luc control mice during their natural lifespan—as a triggering of protein aggregation and clinical disease by the injected α-synucleinhu-MSA. The gene discussed is GFAP; the disease is multiple system atrophy.