Both these outcomes, “autoimmune” and tumorigenesis, may be importantly determined by mitochondrial melatonergic pathway suppression, such as in pancreatic β-cells in T1DM, and in different immune cells (NK cells, macrophages, CD8+ T cells) and/or by increasing AhR/CYP1A2/CYP1B1 and the NAS/melatonin ratio, in cells of the developing tumor microenvironment. This evidence concerns the gene AHR and neoplasm.