We have reported that such crowded cell- like environments dramatically promote fibril formation of the recombinant human PrP and bovine PrP [13,15] and significantly accelerate the nucleation step of fibril formation of the recombinant human PrP and its two pathogenic mutants, CJD-associated E196K and fatal familial insomnia-associated D178N [14]. This evidence concerns the gene PRNP and fatal familial insomnia.