Posterior capsular opacification (PCO) occurs in up to 50% of eyes following cataract extraction1 and its treatment with Nd:YAG capsulotomy is not without complications. PCO also has important implications in the developing world,2 where it may increasingly become a significant cause of treatable blindness. Central to the pathogenesis of PCO is the concept that, following cataract surgery, lens epithelial cells (LECs) migrating from the equator of the capsular bag undergo myofibroblastic or fibroblastic-like change (so called fibrous pseudometaplasia) behind the optic of the intraocular lens (IOL) implant. In order to study the molecular biology of LECs a number of culture methods have been developed. Although many studies have been limited to LECs from animals, it has recently been possible to culture human LECs with both their capsular bag,3 and in a serum free culture medium from age related cataract which closer represents in vitro conditions.4 These cell culture models have been used to assess the pathophysiology of PCO and, in particular, LECs migration, proliferation, and strategies to inhibit these processes. Anti-inflammatory drugs, cytotoxins, antimetabolites, and immunotoxins have all been employed in vitro and in vivo to destroy or suppress LECs.5 Despite attempts at specifically targeting LECs—for example, by utilising monoclonal antibodies, toxic side effects remain the principal limitation in the use of such agents. With the recognition of the role of LECs in PCO, a wide variety of techniques have also been directed at attempting to remove residual cells during surgery. These have included simple aspiration, capsule polishing, ultrasound aspiration, cryocoagulation, and osmolysis.5 The fact that none of these techniques has been utilised as a routine surgical procedure reflects the difficulty in totally removing all LECs. Attempts to remove LECs …