Tg(PrP∆32–80)/Prnp0/0 mice developed disease without elongation in incubation times and accumulated PrPSc∆32–80 in their brains after infection with RML prions (Table 3) [80], suggesting that residues 32–80 are dispensable for PrPC to convert to PrPSc after prion infection. The gene discussed is PRNP; the disease is infection.