Seminal studies on prion disease, undertaken mostly during the second half of the 20th century, have shown that the normal host prion protein (cellular PrP, PrPC) can undergo conformational change, and when misfolded (then referred to as PrPSc) not only causes prion disease in its host but can also under certain circumstances be transmitted to the same or to other species. Here, PRNP is linked to prion disease.