That the nerve lesioning experiments in our study found Sarm1 to drive axon destruction in both young and aged axons suggests it may still be a viable target for both juvenile (i.e. spinal muscular atrophy) and age-associated neurodegenerative disease (i.e. Parkinson’s, Alzheiemer’s, glaucoma). The gene discussed is SARM1; the disease is proximal spinal muscular atrophy.