Current therapies for the prevention of fibrosis after glaucoma filtering surgery can be effective but often produce unwanted side effects. An understanding of the cellular basis of the fibrotic reaction may lead to better treatments. Wound repair revolves around angiogenesis and the activation of fibroblasts by cytokines. These peptides, a number of which have been described, act together in intricately complicated networks to encourage fibroblast chemotaxis, proliferation and contractility, as well as to stimulate the production of glycosaminoglycans and collagen. Since interferons seem to inhibit many of these responses, they deserve further evaluation in the treatment of ocular fibrosis.