It is conceivable that in situations characterized with low Aβ load and tau pathology, as seen in the 11-month-old 3xTg-AD mice, the TfRMAb-TNFR modulates several pathways involved in Aβ formation, microglial function, neurodegeneration, gene expression and autophagy, the positive impact of which becomes evident as the disease progresses. The gene discussed is TNFRSF1A; the disease is Alzheimer disease.