In flies, acetylation of H4K16 on the male X chromosome by MOF in the context of the MSL complex is correlated with transcriptional upregulation as a mechanism for dosage compensation in these organisms. In humans, the MSL complex carries out the majority of genome-wide H4K16 acetylation. In the context of their cognate complexes, Sas2 (SAS) and Esa1 (NuA4) also carry out acetylation of H4K16, in particular in the telomere regions of chromosomes. Sas2 is also observed to acetylate H3K14 "in vitro" on free histones. Esa1 can also acetylate H3K14 "in vitro" on free histones as well as H2AK5, H4K5, H4K8, and H4K12 either "in vitro" or "in vivo" on nucleosomal histones. H2AK7 and H2BK16 are also observed to be acetylated by Esa1 "in vivo". Notably, neither Sas2 nor Esa1 can acetylate nucleosomal histones "in vitro" as a free enzyme. This happens to be the case as well for Sas3, which is observed to acetylate H3K9 and H3K14 "in vivo" as well as lysine residues on H2A and H4. MOZ can also acetylate H3K14.