Transscleral supply of triamcinalone and Lucentis continues to be successfully used in animal models using electrically facilitated macroesis methodology. Nepafenac 4x/day in diabetic subjects for approximately 9 months has shown reductions in cyclooxygenase 2, superoxide, Cyclopamine clinical trial PGE 2, and leukostasis and prevention of functional changes in oscillatory potential along with vasculopathy including regions of acellularity, apoptosis, and degeneration of pericytes. The multi-drug approach might provide the advantage that lower doses of each of the agents could be necessary for efficacy using the good thing about minimizing potential toxicities. This strategy could be justified on evidence that considerable cross-talk of pathways underlie the angiogenic signaling cascade and that the implicit to diabetic retinopathy requires an array of initiators. Especially, beautiful would be the mixtures of mTOR inhibitors with triamcinalone or Retroperitoneal lymph node dissection dexamethasone both which have developed first in class biodegradable system technologies and either scleral or intravitreal sustained drug delivery system for drug delivery to the retina. Several studies have investigated the benefit of combining mTOR inhibitors with proven glucocorticoid antiinflammatory agents in cancer patients. The mTOR inhibitors not merely potentiate the apoptotic influence of steroids, but confer increased sensitivity to glucocorticoids, thereby, potentially allowing continual suitable and chronic use of these drugs in ophthalmology to treat ocular angiogenic and inflammatory diseases with out to boost dosage over time. The clinical utility of glucocorticoids in ophthalmology is substantial but is affected by negative effects as well as the improvement of glucocorticoid resistance imposing a limit to the length of use and clinical utility. The combined utilization of rapamycin with dexamethasone appears to give the advantage of not building resistance to the effects of dexamethasone in addition to improving the proapoptotic caspase 3 signaling. The molecular process by which mTOR inhibitors can augment the pro apoptotic effects of glucocorticoids and consult increased Bicalutamide solubility sensitivity to dexamethasone in a variety of cell lines has been elucidated. Rapamycin promotes the dissociation of the Bim Mcl 1 complex to market dexamethasoneinduced apoptosis and by antagonizing the effect of glucocorticoids to the state of 4E BP1 at Ser65 and p27 upregulation. The mTOR inhibitor CCI 779 in conjunction with dexamethasone also augments the effect of the anti-inflammatory agent. The mixture of mTOR inhibitors with COX2 inhibitors encourages a synergistic effect in suppressing tumefaction angiogenesis which allows subtoxic doses of each agent while retaining efficacy in the clinical management of the disease.