These drug-induced changes are in line with studies by McAlpine and colleagues [25], demonstrating that blockade of TNF-α signaling (either by viral vector-mediated expression of TNFR constructs or by crossing 3xTg-AD mice with TNFR1 knockout mice) significantly suppressed AD pathology. The gene discussed is TNFRSF1A; the disease is Alzheimer disease.