Accordingly, AβOs have been described to activate neuronal JNK and PKR to impair insulin signaling and synapse function (Ma et al., 2009; Bomfim et al., 2012; Lourenco et al., 2013), and transgenic animal models of AD exhibit similar alterations in JNK and PKR activity (Ma et al., 2009; Bomfim et al., 2012; Lourenco et al., 2013). The gene discussed is INS; the disease is Alzheimer disease.