Mounting evidence indicates that misfolded proteins Aβ and Tau can stimulate the immune system to activate resident immune cells such as microglia and astrocytes [111, 112], and to increase retinoic acid-related orphan receptor (ROR)γt+ T cells (Th17) and nuclear factor of activated T (NFAT)c1+ CD4 cells [46], that in turn release inflammatory mediators, ultimately exacerbating AD progression [113, 114]. The gene discussed is CD4; the disease is Alzheimer disease.