In a prior study, we combined ALS case–control exomes with functional assays to demonstrate that a subset of rare variants in the SARM1 gene confer constitutive NADase activity and are greater than 5-fold enriched in ALS patients, supporting SARM1 gain-of-function as a genetic risk mechanism for ALS10. The gene discussed is SARM1; the disease is amyotrophic lateral sclerosis.