Access to genes in DNA is controlled by how tightly DNA is packed in the cell.^1,2 Modification of histones, the proteins around which DNA is wrapped, regulate whether the DNA is accessible to polymerases, allowing the genes to be transcribed, or inaccessible, restricting transcription of genes.^1,2

This epigenetic code is dynamically written, erased, and read by families of enzymes.³ Histone acetyltransferases are writers that add acetyl groups, causing the DNA to become transcriptionally active.^2,3 Histone deacetylases (HDACs) are erasers that remove acetyl groups from histones, resulting in tighter histone-DNA interactions that block gene transcription.^2,3 Readers recognize and bind to modified histones and can recruit transcriptional machinery to certain genes.³

Altered expression, dysregulation, and mutations of HDAC genes leading to alterations in the acetylation state of histones have been implicated in tumor development in various cancers.^2,4,5 Targeting the epigenetic code with molecules such as HDAC inhibitors is a therapeutic approach under active investigation.^1,3