Highly expressed RIPK1 in microglia of human AD brains and an APP/PS1 mouse model is associated with induced CST7 expression, which may be contributed by increased RIPK1 kinase activity in AD, as the pharmacological or genetic inhibition of RIPK1 kinase activity in APP/PS1 mice reduces the DAM phenotype, as illustrated by the decrease of CST7 and restoration of microglial phagocytic activity [44,61]. The gene discussed is CST7; the disease is Alzheimer disease.