Several previous studies have implicated specific signal transduction pathways in the pathogenesis of prion diseases, including the UPR [46], oxidative stress [75], MAPKs [76–78], phosphoinositide-dependent kinase-1 (PDK1) [79], metabotropic glutamate receptors [80], NMDA receptors [81], and voltage-gated calcium channels [82]. This evidence concerns the gene PDK1 and prion disease.