Indeed, Prnp0/0 mice expressing PrP with a deletion of the N-terminal residues 23–31, designated Tg(PrP∆23–31)/Prnp0/0 mice, were shown to be highly resistant to RML scrapie prions, developing disease only after longer incubation times and showing a slower accumulation of pathogenic PrP or PrPSc∆23–31, in the brain after infection with RML scrapie prions [7]. This evidence concerns the gene PRNP and infection.