Consistent with this, in the APP/PS1 mouse model of AD, Dansokho et al. showed that depletion of Tregs accelerated the onset of cognitive deficits triggered by Aβ deposition and that induction of Treg expansion by low doses of IL-2 improved cognitive function in these mice without reducing amyloid plaque burden (17). The gene discussed is IL2; the disease is amyloidosis.