The finding that Trem2 is still induced around residual plaques after early intervention chronic treatment indicates that microglia are capable of actively dealing with Aβ on the long term and suggests that continued dosing with an anti-Aβ antibody could be a valid long-term treatment option, provided that treatment is given at an early time point in amyloid disease stage. The gene discussed is TREM2; the disease is amyloidosis.