To avoid confounding effects of different mouse models, time points of analysis and differences in progression of disease pathology, which in aggressive APP/presenilin overexpressing mouse models may even override microglial amyloid plaque clearance, we choose several independent models to quantitatively investigate TREM2‐dependent antibody‐mediated Aβ clearance under controlled conditions. The gene discussed is TREM2; the disease is amyloidosis.