Recently, it has been reported that repetitive axonal injury in TBI initiates a series of metabolic, ionic, and cytoskeletal disturbances that trigger a pathological cascade, leading to chronic traumatic encephalopathy (CTE) characterized by the accumulation of P-Tau in neurons and astrocytes in a pattern that is distinct from other tauopathies, including AD [98]. The gene discussed is MAPT; the disease is tauopathy.