There are parts of a DNA string that are very susceptible to change. Most of these involve places where the sequences repeat. For example, there is a part of the human genome on chromosome four where the sequence CAG is repeated six or more times. The other strand of DNA in this gene has repeats of GTC. This sequence happens to lie within a gene, called huntingtin.
The two strands of DNA normally bind together because A attracts T and G attracts C. Therefore it is possible for DNA strands with short periodic sequences to bond incorrectly with one strand shifted by three letters from the other. This, of course, leaves a short length of DNA at each end of the repeat segment where the DNA strands cannot bond. But there are repair enzymes which go to work on such mismatched DNA and one possible repair is to splice in an extra CAG on one end of the repeat segment and an extra GTC on the other end. So the repaired DNA molecule would have seven CAG repeats instead of six, and when the cell divides this change is copied.
But the longer the repeat of CAG, the greater is the probability of this mistake happening again, producing a still longer repeat sequence.
When this process runs out of control, the gene may have a very large number of repeats and the protein synthesized using that gene becomes less and less functional. Eventually the person whose DNA has many extra repeats of CAG gets a disease called Huntington's chorea, characterized by a relentless wasting away.
An individual born with extra CAGs in the huntingtin gene is likely to develop Huntington's chorea. The more extra CAGs there are in the gene, the earlier in life the disease will show up.
There are several other human genetic diseases that are also caused by the same kind of repeating sequences in a gene.