Because this resemblance was specific for downregulation, independent of the association of the mutated enzymatic activities with gene activation or repression, we should not consider a priori that these activities were actually deficient in HD; in fact, we were unable to detect a reduction in the levels of the methyltransferases Ezh1, Ezh2, G9a and Hdac1 (Supplementary Fig. S4) to initially support their involvement in transcriptional dysregulation in prodromal stages. This evidence concerns the gene EZH2 and Huntington disease.