Studies in tumor models indicate that this increase in HLA-E is mainly driven by gene transcription mechanisms influenced by cytokines such as tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), and interferon γ (IFNγ) via STAT1-dependent or via Class II transactivator/SXY regulatory pathways (67, –, 69). This evidence concerns the gene TNF and neoplasm.