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Arshad M Khanani,1,2 Matthew W Russell,3,4 Aamir A Aziz,1,2 Carl J Danzig,5,6 Christina Y Weng,7 David A Eichenbaum,8,9 Rishi P Singh3,4 1Sierra Eye Associates, Reno, NV, USA; 2The University of Nevada, Reno School of Medicine, Reno, NV, USA; 3Center for Ophthalmic Bioinformatics, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA; 4Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA; 5Rand Eye Institute, Deerfield, FLA, USA; 6Florida Atlantic University, Charles E. Schmidt College of Medicine, Boca Raton, FL, USA; 7Baylor College of Medicine, Houston, TX, USA; 8Retina Vitreous Associates of Florida, St Petersburg, FLA, USA; 9University of South Florida Morsani College of Medicine, Tampa, FLA, USACorrespondence: Arshad M Khanani 950 Ryland Street, Reno, NV, 89502, USATel +775 329-0286Fax +775-329-0849Email arshad.khanani@gmail.comAbstract: The Ang/Tie2 pathway complements VEGF-mediated activity in retinal vascular diseases such as DME, AMD, and RVO by decreasing vascular integrity, increasing neovascularization, and increasing inflammatory signaling. Faricimab is a bispecific antibody that has been developed as an inhibitor of both VEGF and Ang2 that has shown positive results in phase I, II and III trials. Recent Year 1 data from phase III clinical trials YOSEMITE, RHINE, TENAYA, and LUCERNE have confirmed the efficacy, safety, durability, and superiority of faricimab in patients with DME and nAMD. Faricimab, if approved, may significantly decrease treatment burden in patients with retinal vascular diseases to a greater extent than would current standard of care anti-VEGF injections.Keywords: Ang/Tie, faricimab, YOSEMITE, RHINE, TENAYA, LUCERNE