A prime example of monogenic disorders is the group of over 60 (and still expanding) tandem-repeat disorders, resulting from mutations in over 60 (out of ∼2 million) of the tandem repeats distributed across the human genome.1 Huntington’s disease is a classic example of such a tandem-repeat disorder, and is caused by a cytosine-adenine-guanine trinucleotide (CAG) tandem-repeat expansion in the huntingtin (HTT) gene, encoding an extended polyglutamine tract in the huntingtin protein. The gene discussed is HTT; the disease is juvenile Huntington disease.