In contrast, the CAG/glutamine repeat in the huntingtin (HTT) gene/protein that expands to cause Huntington's disease (HD) is far more polymorphic in the general population, with evidence for functional impacts (short of the HD threshold) of this tandem-repeat polymorphism (TRP) in the non-HD general population [14–17]. The gene discussed is HTT; the disease is juvenile Huntington disease.