Our early detection of PrPSc in the skin of sCJD- and scrapie-infected rodents suggests that it may be possible to do the same with the skin of humans who carry PrP mutations associated with genetic prion diseases such as familial CJD, Gerstmann–Sträussler–Scheinker syndrome, or fatal familial insomnia because it is expected that their mutant PrPC spontaneously converts into PrPSc and accumulates later in life. This evidence concerns the gene PRNP and scrapie.