The PrP-deficient cell models selected for this study were an NMuMG epithelial cell clone, a clone derived from C2C12 muscle myoblasts, and a Neuro2a neuroblastoma cell clone, in which CRISPR-Cas9-based indels in Exon3 led to non-productive PrP expression [7], as well as the 1C11 neuroectodermal cell model exhibiting diminished PrP expression following stable expression of a PrP-specific shRNA [11]. Here, PRNP is linked to neuroblastoma.