In summary, our results in this study suggest that ApoE4 genotype specific PIP2 dyshomeostasis contributes to the development of Tau hyper-phosphorylation after blast TBI exposure, and that elevation of brain PIP2 levels by reducing synj1 expression may ameliorate TBI- associated Tauopathy in ApoE4 carriers. The gene discussed is APOE; the disease is tauopathy.