Halliday et al. (2017) revealed the inhibition of UPR-induced p-eIF2α signaling and neuronal survival by two chemical compounds termed “Trazodone” and “dibenzoylmethane” (DBM) in prion-infected mice (Figure 1, Table 2), presumably by reversing translational attenuation and lowering levels of ATF4 and CHOP which needs to be more inquired in other neurodegenerative diseases including AD and PD. The gene discussed is EIF2A; the disease is Alzheimer disease.