A study by Carling et al. found that APOE ε4 and R47H amplify the tau-induced microglial cGAS-STING-IFN-I responses in female mice, worsening neurodegeneration through upregulated cGAS and BAX-dependent microglial senescence, suggesting that enhanced IFN-I signaling under APOE ε4 and R47H backgrounds could be an important pathological mechanism in AD [181]. The gene discussed is CGAS; the disease is Alzheimer disease.