Tuberculous uveitis has been recognized for a long time (Antoine Maitre-Jan described the first case of iritis associated with tuberculosis [TB] in 1707), and much is understood about its mechanisms. Numerous pathology studies have demonstrated ocular presence of Mycobacterium tuberculosis in cases of uveitis;animal studies have demonstrated that intraocular or miliary M tuberculosis infection will cause uveitic disease. The range of uveitis associated with TB is broad and includes anterior, intermediate, posterior, and panuveitis (including some interesting variants such as serpiginoid uveitis, retinal vasculitis, and choroidal tubercles). While most patients with biopsy-proven tubercular uveitis will have positive tuberculin test results (either the tuberculin skin test or the more recent interferon γ release assays [IGRA] such as QuantiFERON Gold), most patients with tubercular uveitis will have no evidence of pulmonary or other systemic disease. Multidrug treatment of true tubercular uveitis (often with concomitant corticosteroids) will often definitively resolve the uveitis. Conversely, many patients with uveitis will have positive tuberculin test results, particularly in endemic areas: do these patients actually have tubercular uveitis, or do they have 2 independent conditions? Despite near-consensus agreement among experts on these facts, tubercular uveitis remains very challenging to the practicing uveitis specialist. In 2015, the Uveitis Specialists Study Group surveyed the members of the American Uveitis Society, presenting 2 case scenarios and asking members for their estimation of the likelihood of tuberculous uveitis, their preferred workup, and recommended treatment. 1 The group found essentially no consensus among uveitis specialists with respect to any of these questions, with likelihood estimates for a single case ranging from 0% to 90%, and approximately equal numbers of respondents recommending treatment of 6, 9, and 12 months for TB in likely cases. Later, a second group of primarily non-US-based physicians was given the same set of scenarios. Their assessments, workup, and suggested treatments were also highly variable and in many cases significantly different from those of US-based specialists. 2 This difficulty arises from the lack of a gold standard diagnostic test for tubercular uveitis. It is believed that much of the uveitis associated with tuberculosis is caused by innate and adaptive immune responses to tubercular antigens as much as to the organism itself. As such, very small bacterial loads, perhaps as low as a single bacillus, 3 can induce substantial inflammation. While the polymerase chain reaction has been successfully used in many cases to diagnose tubercular uveitis, its false-negative rate is unknown; a negative result does not rule out tubercular disease. In the absence of a definitive laboratory test, the presence of a compatible form of uveitis and a positive skin or IGRA test result is taken as presumptive diagnosis for tubercular uveitis.