Recently, researchers have focused on calcium dyshomeostasis based on the following evidence: 1) Nav1.6 enhances BACE1 transcription via regulating Na+ influx; 2) dysfunction of Nav1.6 in the injured axons induces Ca2+ influx via reversing the Na+‐Ca2+ exchanger (NCX) (Alrashdi et al., 2019; Craner et al., 2004; Omelchenko et al., 2019); and 3) elevated intracellular Ca2+ is an early pathological factor of AD and accelerates Aβ production, which is derived from the observation in AD patient brains (H. J. Cho et al., 2008; Demuro et al., 2010; Ishii et al., 2019). The gene discussed is TLX2; the disease is Alzheimer disease.