Corneal fibrosis contributes to the substantial health burden due to “corneal blindness”, a leading cause of blindness world-wide. Molecular intra-cellular regulators of the cytoskeleton, suggests that this class of proteins may be targets for therapeutic development. In the transformation the usually quiet fibroblast-to-a myofibroblast morphology, the expression of α-smooth muscle actin (SMA) is characteristic. As an excessive healing response, fibrosis is the result of the corneal keratocyte to myofibroblast transformation and may occur in response to trauma, infection as well as surgery. Using a mouse model of fibrosis following both infection with Pseudomonas and by trauma (an anterior keratectomy) it was shown using an array for the cytoskeletal regulators that one key molecule was highly unregulated. Moesin a member of the ERM Complex (ezrin/radixin/moesin) was highly unregulated. The use of siRNA applied by iontophoresis showed that the molecules characterizing fibrosis, such as alpha-SMA. The clinical development focuses on a method that can be applied topically to lessen or prevent fibrosis after corneal insult.