The development of novel AD therapeutic approaches may benefit from further research on the upstream signals that stimulate Notch receptor protein upregulation, the molecular mechanisms that activate the AHR signaling pathway to inhibit the response of ILC2s, strategies to effectively reduce the expression of GzmB or decrease the degradation of E-cadherin in AD patients, and the role of antagonizing the effect of CRTH2 on ILC2s. The gene discussed is CDH1; the disease is Alzheimer disease.