Current AD animal models have shifted from single genetic mutation models to multi-gene transgenic models, and consider non-genetic pathogenic factors and species differences to more accurately simulate the AD progression process.484–487 While immunotherapy appears to be the most advanced therapeutic strategy, primarily targeting traditional targets such as Aβ and tau, a noticeable paradigm shift is occurring toward small-molecule therapeutic modalities.435 These modalities, characterized by their simplicity, maturity, and adaptability, provide a promising avenue for emerging targets. The gene discussed is MAPT; the disease is Alzheimer disease.