Notably, genetic or pharmacologic inhibition of the necroptosis mediators RIPK1 kinase activity, RIPK3, or MLKL demonstrates therapeutic benefit in mouse models of inflammatory bowel disease, ischemia–reperfusion injury, drug-induced liver injury, acute kidney injury, retinal detachment, chronic dermatitis, atherosclerosis, and amyotrophic lateral sclerosis (ALS)6,7. Here, RIPK3 is linked to amyotrophic lateral sclerosis.