To investigate how SET protein accumulation influences the epigenetic control of gene expression, we analysed the DNA methylation profile in two non-tumour cell lines, HEK293 and NOK-SI, with and without SET overexpression (HEK293/SET and NOK-SI/SET, respectively), and three HNSCC cell lines, HN6, HN12, and HN13, which present SET constitutively accumulated [15], with and without SET knockdown (HN6siSET, HN12siSET, and HN13siSET, respectively). The gene discussed is SET; the disease is neoplasm.