In particular, it was demonstrated that rapamycin reduces the deposition of amyloid plaques and delays symptoms' onset in transgenic mice that express a mutant PrP (A116V), associated with an inheritable form of GSS (Cortes et al., 2012), and restored autophagy flux in neuroblastoma cells incubated with a cytotoxic recombinant PrP-derived peptide (Thellung et al., 2018). Here, PRNP is linked to neuroblastoma.