Therefore, prior to interpreting the results of a genetic cross to determine whether heterozygous knock-down of Hdac7 has a beneficial effect on R6/2 HD-related phenotypes, it was important to show that (1) Hdac7 expression is reduced in Hdac7+/− knock-out mice: that Hdac7 is not auto-regulated to wild type levels as is the case for Hdac1[38] and (2) that the presence of the R6/2 transgene does not alter Hdac7 expression levels. Here, HDAC1 is linked to Huntington disease.