Despite the many advances in the therapy and diagnosis of primary open angle glaucoma, and the recognition of intraocular pressure as the major modifiable risk factor,1 2 the pathogenesis of the disease still remains unclear. The most pathognomonic feature of glaucoma is optic disc cupping and the primary site of glaucomatous optic nerve damage appears to be at the optic nerve head.3 However, the exact mechanisms by which this damage occurs have not been elucidated. Changes in lamina cribrosa morphology and nerve fibre bundle pore morphometry4 5have been documented in this disease, in association with alterations in the surrounding extracellular matrix.6-11 The tortuous course of the individual nerve fibres may also play a role.12 In this issue of theBJO (p 209), Pena et al have found that the production of a growth factor, transforming growth factor β (TGF-β2) is considerably increased in the optic nerve heads of patients with open angle glaucoma but not in normal individuals. This finding is important because of its implications for the pathogenesis of glaucomatous damage. Like all interesting research findings, it raises further intriguing questions. Is TGF-β2 stimulated in response to nerve axon loss or changes in extracellular …