The monogenic autosomal-dominant nature of Huntington’s disease, associated with the cytosine-adenine-guanine (CAG) trinucleotide repeat encoding an expanded polyglutamine tract in the huntingtin protein, means that the children of those with the gene mutation face the ‘flip of a conceptual coin’, affecting whether they will suffer from this currently incurable disease (after receiving the tandem-repeat expanded Huntington’s disease allele from one of their parents) or escape such a dreadful fate. Here, HTT is linked to juvenile Huntington disease.