The ocular tissue is one of the most densely populated tissues in the body with extremely small blood vessels, and vascular lesions have been reported to be a factor in vision loss and visual field defects in many ocular diseases. Currently, vascular endothelial growth factor (VEGF)-targeted agents are the first line of treatment for intraocular vascular lesions, however, there are some cases in which they are not fully effective. Therefore, exploring pathogenesis molecules other than VEGF and identifying target molecule-selective therapies may help to solve the problem. Through experimental pathological models that mimic intraocular vascular lesions, we have been investigating factors that maintain the physiological balance of blood vessels and analyzing their functions. In this symposium, we will focus on the Bric-a-brac, Tramtrack, and Broad Complex (BTB) proteins. Using an intraocular vascular lesion model, we found that ankyrin repeat and FYVE domain containing 1 (ANKFY1) and B-cell CLL/lymphoma 6 member B protein (BCL6B) play important roles in neovascularization and hyperpermeability. Whether ANKFY1 and BCL6B may be a new therapeutic strategy to complement the disadvantages of anti-VEGF therapy will be discussed as a potential therapeutic target of BTB proteins for intraocular vascular lesions.