Sporadic CJD occurs most frequently in MM homozygous individuals and it is also relevant in the acquired forms of CJD, most strikingly in vCJD, where most clinical cases studied so far have been homozygous for methionine at codon 129 of PRNP. A polymorphism at codon 127 (G127V) of PRNP has recently been determined as a resistance factor against the kuru epidemic and this observation also dismissed speculations of possible pathogenic mutation that could have triggered the kuru outbreak [120]. This evidence concerns the gene PRNP and Creutzfeldt Jacob disease.