However, the assumption that anchorage by GPI and residence at lipid rafts of PrPC supports its misfolding into PrPSC and the development of infectious scrapie disease is apparently in contradiction to the observation that PrPC with missing GPI anchor was produced and propagated with significantly higher efficacy in vivo with accompanying elevated risk for the transmission of prion diseases [101]. This evidence concerns the gene PRNP and prion disease.