Several lines of evidence obtained in AD mouse models suggest that soluble Aβo alter the excitation/inhibition balance by decreasing the inhibitory GABAergic function, which in turn induced an excessive activation of the excitatory glutamatergic system in AD mice (Busche et al., 2008; Palop and Mucke, 2010; Busche and Konnerth, 2016; Styr and Slutsky, 2018). The gene discussed is ABO; the disease is Alzheimer disease.