EZH1 and Huntington disease: 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.