Overall, the accumulating evidence on α4 or β2 KO protection in Tg AD models is at odds with the multiple studies on the detrimental effects of β2* nAChR loss on several types of lesion and neurodegeneration (Zoli et al., 1999; Laudenbach et al., 2002; Bao et al., 2005; Zanardi et al., 2007; Huang et al., 2011; Konsolaki and Skaliora, 2015). The gene discussed is CHRNA4; the disease is Alzheimer disease.