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. This evidence concerns the gene DDIT3 and Parkinson disease.