Indeed, while in some of these patients pure GSS histopathological features correlate with the presence of the GPI-anchorless PrP fragment, in others mixed CJD/GSS features (e.g., widespread spongiform changes cooccurring with amyloid plaques) correlate with the deposition of both types of PrPSc forms (e.g., GPI-anchored and glycosylated N-terminal PrPSc fragment + truncated internal PrP fragments lacking the GPI anchor). This evidence concerns the gene PRNP and Creutzfeldt Jacob disease.