Conversely, we observed decreased levels of p-Akt Ser473, p-mTOR Ser2448, and mTOR activity concomitant with the decline of tauopathy and neuronal loss at 30 days post-ischemia in the absence of changes in Bcl-2 protein levels, suggesting apoptotic regulation (Iadecola and Anrather, 2011). The gene discussed is MTOR; the disease is tauopathy.