In view of the aforementioned easy transmissibility of other human prion diseases, the barrier appears to be conformational rather than caused by species-related variations in amino acid sequence of PrPC (15,16); the barrier might be associated with the misfolding of VPSPr PrPD, which may be peculiar because after PK digestion it results in an array of highly heterogeneous fragments and apparently the failure to convert one of the glycoforms (6,7). Here, PRNP is linked to prion disease.