The results showed that these transgenic mice exhibited no AD‐like pathology, and displayed comparable levels of Nav1.6 both in the whole cell and the cell surface at 2–3 months of age (Figure 1), whereas significant elevated levels of Nav1.6 in the whole cell fractions and the cell surface were observed in the brains of APP/PS1 mice compared to the WT mice at 7–8 months of age, the time when APP/PS1 mice harbored extensive Aβ plaques and showed cognitive deficits (Zhang et al., 2014). This evidence concerns the gene SCN8A and Cognitive impairment.