A recent study on Huntington’s Disease showed that overexpression of different mutant polyQ Huntington transgenes in circadian clock neurons induces circadian arrhythmicity and aggregation of Htt-polyQ in small ventral lateral neurons (sLNVs) as well as reduction in cell numbers indicative of cytotoxicity (Xu et al. 2019a, 2019b). Here, HTT is linked to juvenile Huntington disease.