Emerging evidence demonstrates the therapeutic promise of second-generation JAK inhibitors (e.g., deuruxolitinib, brepocitinib) in AA-AD comorbidities, yet critical gaps persist in delineating their tissue-specific JAK-STAT pathway modulation and optimal dosing schedules, requiring validation through multicenter Phase IIIb trials coupled with longitudinal biomarker profiling (Figure 4). The gene discussed is SOAT1; the disease is Alzheimer disease.