Mali Jiang et al. discovered that Nemo-like kinase (NLK) interacts with HTT and that NLK levels are significantly reduced in HD human brain and HD models, demonstrating that NLK overexpression in the striatum reduces brain atrophy and mutant HTT(mHTT) aggregation in HD mice, lowers mHTT levels in a kinase activity-dependent manner while having no significant effect on normal HTT protein levels, and promotes mHTT ubiquitination and degradation via the proteasome pathway, suggesting a protective role of NLK in HD and identifying a new molecular target to reduce mHTT levels [86]. This evidence concerns the gene HTT and Huntington disease.