Recent work in neurodegenerative disease populations shows that biomarkers like phosphorylated tau (e.g., P-tau181, P-tau217) [19] and glial fibrillary acidic protein (GFAP) are relatively specific to the Aβ-mediated components of AD pathophysiology [20–23] that presumably are distinct from CTE, including in patients with TES [19]. The gene discussed is GFAP; the disease is Alzheimer disease.