It is worth mentioning that overexpression of TRIM11 may lead to tumor growth, migration, and invasion in glioma.4 The oncogenic feature of TRIM11 and its potential in AD treatment provide strong evidence that an imbalance of damage and repair drives disease and aging.5 Moreover, it should be extensively and critically evaluated whether upregulation of TRIM11 would present impressive efficacy in the prevention and treatment of AD in humans. The gene discussed is TRIM11; the disease is central nervous system cancer.