In our study, estrogen led to α7nAChR overexpression and reduced proinflammatory cytokine levels in the serum, supporting the enhancement of cholinergic anti-inflammatory signaling; moreover, dysfunction of ABR alleviated these estrogen effects, suggesting that the downstream cholinergic anti-inflammatory signaling participates in estrogen-mediated protection against stroke. The gene discussed is CHRNA7; the disease is stroke disorder.