Duplication would be expected to increase prion protein (PrP) expression by up to 1.5 times; transgenic mice engineered to overexpress Prnp (>8 times) do not develop clinically evident spontaneous prion disease in their normal lifespan, despite having very short incubation times when inoculated with prions (Fischer et al., 1996). This evidence concerns the gene PRNP and prion disease.