The presence of both cholinergic (ACHE/CHRM1) and redox-inflammatory (NOS1/NOS2; PTGS1/ALOX5/PLA2G2A) cores supports a multi-target strategy that has been repeatedly highlighted as more suitable for AD than single-node blockade, because synaptic loss is reinforced by feedback loops between ROS/RNS damage and microglia-mediated inflammation [16,17]. The gene discussed is PLA2G2A; the disease is Alzheimer disease.