<p>DNA methylation of tumour suppressor genes is the most well-studied epigenetic alterations in head and neck cancer. The tumour suppressor genes <i>CDKN2A, RASSF1,</i> and <i>TIMP3</i> are the most frequently investigated, but the methylation status has been analysed in more than another dozen genes, for example <i>MGMT</i>. In oral squamous cell carcinoma (OSCC) methylation of <i>MGMT, DAPK</i>, and <i>CDKN2A</i> are promising biomarkers of prognostic value. Inhibition of <i>LSD1</i>, encoding a histone demethylase, attenuates the development and growth of OSCC. Methylation of <i>TIMP3</i> in sinonasal adenocarcinoma (intestinal type) is associated with a significant worse survival, an association not seen in sinonasal squamous cell carcinoma. Olfactory neuroblastoma can be distinguished into four unique subgroups by methylation profiling. Methylation of <i>RASSF1</i> is seen in NUT carcinoma, and significantly higher <i>RASSF1</i> methylation is found in SMARCB1/INI1-deficient tumours compared to the less aggressive SMARCB1/INI-proficient tumours. Genome-wide methylation profiling in combination with <i>IDH2</i> mutation status suggests that tumours with undifferentiable SNUC morphology can be classified into for subgroups. Most salivary gland carcinoma subtypes have specific epigenetic signatures. Four of the most common subtypes, adenoid cystic carcinoma (ADCC), mucoepidermoid carcinoma (MEC), acinic cell carcinoma (ACC), and carcinoma ex pleomorphic adenoma (CXPA) have all methylation of <i>RASSF1A</i>, two (MEC and ADCC) also of <i>TIMP3</i> and two (MEC and CXPA) of <i>p16INK</i>^<i>4a</i>. A methylation landscape of 20 salivary gland tumours (SGTs) is nowadays available.</p>