NLK and amyotrophic lateral sclerosis: Because no known neurological condition in humans has been associated with a reduction of Nlk, mice with partial genetic reduction of Nlk display no pathological (neurodegenerative or inflammatory), survival, or cognitive changes up to 52 weeks (57), and mice with postnatal whole-body conditional ablation of Nlk are grossly normal (57), we believe targeted reduction of Nlk or its downstream effectors to increase ALP function is a potentially generalizable therapeutic strategy for several neurodegenerative disorders, beyond just ALS.