In the past 3 years, seven human neurological disorders have been foun
d to be associated with an abnormal number of unstable trinucleotide r
epeats within exons or non-expressed regions of a gene. These forms of
mutations are called dynamic mutations. The expansion in copy number
of trinucleotide repeats may represent a large number of hereditary di
sorders. The correlation between the length of the repeated size and t
he disease severity and variable onset has provided some genetic expla
nation for a phenomenon called anticipation. However, there are numero
us questions which cannot be explained by anticipation. Many other fac
tors such as genomic imprinting and variable DNA methylation may also
contribute to the puzzling features of these phenotypes.