In human PRNP, the widely-studied A117V mutation, and a variety of synthetic alanine to valine mutations at 4 other positions in the hydrophobic tract increase biogenesis of a transmembrane form of the protein (“CtmPrP”), and may be a cause of Gerstmann–Straussler Syndrome and neurodegenerative disease in transgenic mice, respectively [23]. This evidence concerns the gene PRNP and neurodegenerative disease.