The only biochemical feature that was apparently conserved in all BSE-derived prions after passage in the different species was the lack of reactivity of PrPres to the N-terminal binding antibody 12B2 (Figure 1), indicating that the characterization of the abnormal PrP N-terminal truncation by PK could remain a robust approach for potential BSE agent identification when screening TSE isolates from different species. This evidence concerns the gene PRNP and human prion disease.