Gene and thus protein expression are tightly controlled by the DNA sequence and are susceptible to mutational changes that are irreversible. However, the epigenetic code is independent of the DNA sequence, is heritable and reversible, and often greatly influences gene expression. Therefore, in addition to a genetic influence, epigenetic dysregulations closely tie to the initiation, progression, and metastasis of cancer by influencing pathways that regulate cell division, cell proliferation, and cell death. Analysis of the epigenomes has unraveled the primary mechanisms of gene regulation by epigenetics and includes DNA methylation, histone modifications, and noncoding RNAs such as microRNAs (miRNAs). However, newer molecules and structures have also been identified in the process of epigenetic control of diseases and include long noncoding RNAs (lncRNAs) and exosomes, respectively. Through these mechanisms, gene expression is influenced by the type of epigenetic code such as methylation marks, histone acetylation, or miRNAs impacted. Either targeting enzymes that regulate these processes or manipulating the structures (exosomes) that carry modifiers such as miRNAs can serve as suitable therapeutic strategies in cancer. Here we review current approaches to targeting enzymes such as the DNA methyltransferases, histone acetyltransferases, histone deacetylases, histone methyltransferases, and histone demethylases that regulate epigenetic pathways through drug-based inhibitors. Additionally, the impact of miRNA expression (up- or downregulation) and lncRNA will be broadly covered. Exosomes, nanosized particles that are known to deliver miRNAs or lncRNAs to target cells by cancer cells that aid in the progression and metastasis of the disease, will be also reviewed.