(iii) CDK5 promoted the aberrant hyperphosphorylation amyloid precursor protein, tau, and neurofilament, which contributed to the formation of neurofibrillary tangles, synaptic damage, mitochondria dysfunction to cell cycle reactivation, and neuronal cell apoptosis in AD (Patrick et al., 1999; Liu et al., 2016); besides, CDK5 hyperactivation might trigger glia to produce proinflammatory cytokines and chemokines by regulating cPLA2, which contributed to neuroinflammation; thereby, CDK5 inhibition repressed cell apoptosis and inflammation in AD (Sundaram et al., 2012). The gene discussed is CDK5; the disease is Alzheimer disease.