However, that being what it may, the original studies and their conclusions seem to be consistent with mounting evidence that supports a role for repetitive axonal injury from concussions, with and without clinically evident symptoms, and the consequent downstream neuroimmune activation, ionic shifts, and cellular flux has on toxic proteinopathies such as amyloid beta (Aβ), tau and TAR DNA-binding protein 43 (TDP-43), cognitive dysfunction, and impaired neurotransmission that are features classically seen in CTE (2). The gene discussed is TARDBP; the disease is proteostasis deficiencies.