In contrast, Tg(FFI) mice expressing mutant PrP at twice the endogenous level or more developed a progressive and invariably fatal neurological disease, and accumulated detergent-insoluble, protease-resistant PrP in their brains, yielding a 19 kDa C-terminal fragment after mild PK digestion and deglycosylation, like in FFI patients.7 The gene discussed is PRNP; the disease is nervous system disorder.