Second, the atomic structure of wild-type PrP fibrils has shown that several familial mutations including K194E, E196K, and E211Q may break salt bridges essential for forming the protofilament interface in wild-type PrP fibrils and thus disrupt PrP fibril structure (33), but whether genetic prion disease–related mutation E196K displays a new amyloid fibril structure is unknown. Here, PRNP is linked to prion disease.