However, by 9 months of age, a sharp decline in HIF-1α and mTOR activity was observed, indicative of an immune-suppressed state resembling the chronic phase described by Baik et al. In this context, PDCs treatment successfully restored mTOR-HIF-1α signaling, leading to improved microglial function and neuroprotection in advanced-stage AD [306]. The gene discussed is MTOR; the disease is Alzheimer disease.