Epigenetics—the study of the layer of gene regulation not accounted for by the DNA sequence itself—is a burgeoning field increasingly tied to diseases such as cancer and Alzheimer’s disease in humans. A prevailing avenue of current research is the so-called histone code—the large number of posttranslational modifications (PTMs) made to the histone proteins around which DNA is wrapped. These PTMs act in a highly specific and often synergistic manner to promote or repress transcription of DNA proximal to the histone. The histone code is created and managed by families of enzymes that are either readers or writers of histone PTMs. Dysregulation of the activity of these proteins can cause disease. The effects of the majority of histone PTMs are currently unknown. A method to cause targeted, specific epigenetic modifications in human cells would be a great asset for investigating the effects of each histone modification, and to observe phenotypes resulting from the editing of histone PTMs at specific loci. Work presented in this thesis attempted to develop such a method using a dCas9 targeting system with a histone lysine methyltransferase, SETD7. Non-specific histone modification was achieved in solution, and attempts were made to test these reagents in mammalian cells. However, constructs designed for increased specificity did not cause histone PTMs either in solution or in mammalian cells. Work was also undertaken to aid the development of inhibitory drug candidates for the extraterminal (ET) protein-protein interaction domain of Brd3, a clinically significant histone PTM reader that is dysregulated in numerous cancers. Candidate small molecule inhibitors were investigated by nuclear magnetic resonance spectroscopy (NMR). NMR binding data showed that the drug candidates are tight binders of the Brd3 ET domain, and molecular docking demonstrated that at least one candidate might act as a competitive inhibitor of the native ligand. Overall, this work provides progress towards both the study of histone regulation and the treatment of its dysregulation