AKT1 and Alzheimer disease: This suggests that the stability of FOXP3 expression in Tregs is not linked to and does not promote cell survival.64 Furthermore, expression of ICOS by Tregs can generate instability and reprogramming through the PI3K/AKT pathway, which, in turn, is detrimental to their suppression activity.19 Thus, ICOS+ Treg viability may be impaired upon restimulation in patients with AD, hence impeding their production of IL‐10 and, in turn, the efficacy of their immunosuppression.