Interferons (IFNs) comprise a family of secretory proteins induced in response to specific extracellular stimuli through stimulation of toll-like receptors (TLRs). Acting in paracrine or autocrine modes, IFNs stimulate intra- and intercellular networks for regulating innate and acquired immunity, resistance to viral infections, and normal and tumour cell survival and death. Through high-affinity cell surface receptors IFNs stimulate genes, using signalling molecules used by other cytokines, but first identified through studies of IFNs. Perturbations in these pathways can lead to overstimulation of cellular functions or can make cells resistant to a given ligand, facilitating either progression or resistance of malignancy. IFNs act on almost every cell type and through their cellular actions can be effective in inhibition of tumour emergence, progression, and for inducing regression. Interferon has historical significance as a possible treatment for carcinoid tumors, but its toxicity and relative lack of efficacy limit its use. In early trials, response rates ranged from 20% to 55%, with response gauged by decrease in symptom burden rather than radiographic response. Little radiographic response has been shown with interferon. Patients with carcinoid tumors treated with interferon may develop a wide variety of autoimmune diseases, such as thyroid disease (thyrotoxicosis, hypothyroidism), pernicious anemia, and vasculitis. Accounting for these toxicities, the lack of significant benefit, and the presence of more effective therapies, the use of interferon for carcinoid tumors is not common.