A white man in his early 80s with history of autoimmune pancreatitis, recurrent colon polyps, and benign prostatic hyperplasia developed rapid, painless vision loss of both eyes over a 2-week period 6 months after cataract surgery. Vision was 20/250 OD and 20/60 OS. The anterior segment was unremarkable in either eye, while the posterior segment examination noted 1+ vitreous cell, asteroid hyalosis, and a multilobulated, serous retinal detachment (RD) in the right eye and trace vitreous cell and a multilobulated, serous RD in the left eye. Imaging included B-scan, optical coherence tomography, and fundus autofluorescence, which revealed diffuse choroidal and ciliary body thickening, multifocal pockets of subretinal fluid, and speckled hyperautofluorescence and hypoautofluorescence in both eyes (Figure 1). No poliosis or skin changes were noted. A review of systems was unremarkable, most notably a lack of any pulmonary symptoms. A focused laboratory evaluation identified a significantly elevated angiotensin-converting enzyme (ACE) level and antinuclear antibody titer, but serum lysozyme, syphilis, and tuberculosis testing had negative results. To better differentiate between Vogt-Koyanagi-Harada (VKH) syndrome, a lymphoproliferative disorder, or sarcoidosis as the underlying cause of the vitreous inflammation and multilobulated, serous RD in both eyes, a computed tomographic scan was performed. It showed marked lymphadenopathy throughout the mediastinum and diffuse scleral thickening in both eyes. The institute’s radiologists believed these computed tomography findings were nonspecific and could be indicative of either sarcoidosis or intraocular lymphoma.