Mechanistic studies establish RIPK1-driven necroptosis as clinically relevant in neurological pathologies: In Alzheimer’s disease models, pharmacological inhibition of RIPK1 by necrostatin-1 attenuates tau hyperphosphorylation and Aβ-induced neuroinflammation while rescuing cognitive impairment in APP/PS1 mice (Yang et al., 2017). The gene discussed is RIPK1; the disease is early-onset autosomal dominant Alzheimer disease.