In chronic AD lesions, there is an intensification of T-helper cell type 2 (Th2) and Th22 responses along with the concurrent activation of the T-helper cell type 1 (Th1) axis that results in increased levels of interferon-gamma (IFN-γ), chemokine (C-X-C motif) ligand 9 (CXCL9), and chemokine (C-X-C motif) ligand 10 (CXCL10), rather than a complete shift to a Th1-only signature [48,49,50]. The gene discussed is CXCL10; the disease is Alzheimer disease.