Extensive studies have shown that inhibition of RIPK1 kinase activity by the chemical compound necrostatin-1 or by knock-in of a kinase-dead form of RIPK1 can ameliorate necroptosis-associated pathologies in mouse models of various diseases, including inflammatory diseases (e.g. colitis and dermatitis) and in neurodegenerative diseases (e.g. multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS))24,25. The gene discussed is RIPK1; the disease is amyotrophic lateral sclerosis.