Additionally, the comparison of our data to gene dysregulation in the striatum of CHL2 knock-in mice versus that of R6/2 transgenic mice further indicated that our dataset contains information relevant to HD target selection as illustrated by the proposed inhibition of phenylalanine-4-hydroxylase as a candidate strategy to reduce early HD phenotypes that may be associated to a transient excess of dopamine [49]. This evidence concerns the gene PAH and Huntington disease.