Simple Summary Epstein-Barr Virus (EBV)-induced lymphomas have a significant global incidence, given the widespread infection to the human population. EBV adopts several mechanisms to replicate and persist in the host, by hijacking its epigenetic machinery. The main topic of this review details the current insights of EBV interactions with the host epigenetic system, and it will be discussed the potential relationship between the EBV-induced chronic inflammation and the dysregulation of epigenetic modifiers that might lead to tumorigenesis. Promising novel therapies against several types of cancer involve the use of epigenetic modifier inhibitors. To design new therapeutical strategies targeting lymphomas, it is crucial to conduct exhaustive reaserch on the regulation of these enzymes. Abstract During the past decade, the rapid development of high-throughput next-generation sequencing technologies has significantly reinforced our understanding of the role of epigenetics in health and disease. Altered functions of epigenetic modifiers lead to the disruption of the host epigenome, ultimately inducing carcinogenesis and disease progression. Epstein–Barr virus (EBV) is an endemic herpesvirus that is associated with several malignant tumours, including B-cell related lymphomas. In EBV-infected cells, the epigenomic landscape is extensively reshaped by viral oncoproteins, which directly interact with epigenetic modifiers and modulate their function. This process is fundamental for the EBV life cycle, particularly for the establishment and maintenance of latency in B cells; however, the alteration of the host epigenetic machinery also contributes to the dysregulated expression of several cellular genes, including tumour suppressor genes, which can drive lymphoma development. This review outlines the molecular mechanisms underlying the epigenetic manipulation induced by EBV that lead to transformed B cells, as well as novel therapeutic interventions to target EBV-associated B-cell lymphomas.