Changes in gene expression and activity underlie the formation of cancerous tumors. Historically, alterations (deletions, point mutations, translocations, etc.) in the DNA genome of the cell were believed to be the basis for tumor formation, but recent studies have demonstrated that epigenetic modifications, which involve the regulated addition of chemical groups to DNA and histones, also profoundly affect gene expression and, thus, cancer. Both genomic region compaction and gene expression are modulated by epigenetic modifications, which are deposited by specific enzymes (known as "writers"), and subsequently recognized by effector proteins ("readers"). Most, if not all, epigenetic marks are reversible, and various enzymes ("erasers") remove these marks. The complex interplay of these three classes of proteins controls gene transcription, and defects in this system contribute to cancer initiation and progression. This chapter will introduce the key concepts surrounding these three types of proteins, with a particular focus on methyl and acetyl marks.