To prove that the disturbed acetylation status of H3K14 lysine plays a role in mediating the effects of altered HAT and/or HDAC activity upon mHtt-induced stress, we tested the genetic interactions of His3.3A-K14 mutant transgenes and loss-of-function mutants of the HAT Gcn5 and the HDAC Sirt1 in the HD model. This evidence concerns the gene KAT2B and Huntington disease.