So far, the etiology of AD is not fully understood, but several common hallmarks, including cholinergic dysfunction (Scarpini, Scheltens & Feldman, 2003), amyloid-β (Aβ) deposits (Terry, Gonatas & Weiss, 1964), τ-protein aggregation (Grundke-Iqbal et al., 1986), oxidative stress (Wilson et al., 2013), neuroinflammation (Linker et al., 2011), excitotoxicity (Kaidery et al., 2013), calcium impairment (Diaz et al., 2009), mitochondrial dysfunction (Aliev et al., 2014), have been reported to tightly correlated to the development of AD. The gene discussed is TBXT; the disease is Alzheimer disease.