This literature marketed report as received from the authors of the published literature article, titled as stated above, refers to a 43-year-old male patient with type 2 diabetes mellitus. On an unknown date, the patient was vaccinated with his first dose of single-antigen hepatitis B vaccine (recombinant) (manufacturer unknown) (route of administration, dose, lot # and expiry date were not reported) for prophylaxis. Three days after receiving the vaccine, he developed decreased vision, photophobia, and redness in both eyes. He was initially diagnosed with anterior uveitis by an outside specialist and treated with topical prednisolone acetate 1%. One week later, he developed sudden loss of vision in the right eye and was referred to the authors' service for further management. On presentation, best corrected visual acuity was 20/800 in the right eye and 20/40 in the left eye with intraocular pressures of 18 and 12 mmHg, respectively. Anterior segment exam was notable for trace cell with pigment on the anterior lens capsule in the right eye and trace cell with scattered posterior synechiae and pigment on the anterior lens capsule in the left eye. There were trace cells in the anterior vitreous of both eyes without vitreous haze. Funduscopic examination showed disc edema with numerous deep creamy-white lesions in the posterior pole of both eyes. Enhanced depth imaging (EDI) with spectral domain optical coherence tomography (OCT) demonstrated marked choroidal thickening that was more prominent in the right eye with choroidal undulation and sub-retinal fluid accumulation. OCT also showed sub-retinal septae with associated cystic cavities. Wide-field fluorescein angiography (FA) demonstrated early hypofluorescence with late hyperfluorescence of the placoid lesions, along with several pinpoint leaks in the posterior pole. Indocyanine green angiography (ICG) demonstrated hypocyanescent lesions in early and very late phases. Review of systems was unremarkable, and diagnostic work-up, including interferon gamma release assay, angiotensin-converting enzyme, Treponemal IgG, bartonella serologies, human leukocyte antigen (HLA) testing, and chest x-ray, were all unremarkable. The patient was treated for non-infectious panuveitis with choroiditis with a daily dose of 100 mg of oral prednisone (1 mg/kg body weight), topical prednisolone acetate 1%, and cyclopentolate 1%. Vision and retinal anatomy improved dramatically within days of initiating systemic corticosteroid treatment. Two months after initial presentation, visual acuity had improved to 20/30 in both eyes with normalization of retinal anatomy on OCT. We advised the patient against completing the hepatitis B vaccine (recombinant) (manufacturer unknown) vaccine series. The patient was then lost to follow-up and re-presented 5 months later, due to recurrent symptoms. In the interim, he reported two flares during which he self-treated with oral and topical steroids for 3 days each with resolution. Review of systems was now significant for tinnitus and headaches. On re-evaluation of family history, the patient reported paternal ancestors. Inspection of the skin showed hypopigmented areas on the chin consistent with vitiligo. Best corrected visual acuity was 20/25 in both eyes. Funduscopic examination revealed recurrent disc edema bilaterally with new deep creamy-white lesions in the posterior pole of both eyes. A peri-papillary choroidal neovascular membrane (CNVM) was present in the right eye. Computed tomography of the chest showed mediastinal lymphadenopathy and an 8 mm lung nodule. A lumber puncture was normal without cerebrospinal fluid (CSF) pleocytosis or malignant cells. A clinical diagnosis of VogtKoyanagiHarada (VKH) disease was made and intraocular inflammation was controlled with oral corticosteroids followed by methotrexate for long-term disease control. The CNVM resolved with one treatment of intravitreal bevacizumab (1.25 mg/0.05 cc). The patient was referred to pulmonology and evaluation was not consistent with sarcoidosis. The outcome of VKH disease was considered as recovered/resolved with sequelae. The reporters considered VKH disease to be associated with hepatitis B vaccine (recombinant) (manufacturer unknown). They reported that the mechanism of vaccine-associated uveitis was unclear and it is difficult to assert causality in these rare cases. One proposed mechanism is related to the use of adjuvants in vaccines, since adjuvants enhance immunogenic activity by a combination of mechanisms, including cytokine and chemokine release, sustained release of antigen (depot effect), activation of antigen presenting cells, antibody production, and cellular recruitment. The authors concluded that while the underlying etiology remained unclear, VKH disease could be associated with a viral prodrome suggesting an infectious trigger that altered the immune response. Although it was difficult to determine causality, this case raised the possibility of hepatitis B vaccine (recombinant) (manufacturer unknown) vaccination triggering VKH disease in a susceptible individual.Upon internal review, the event of VKH disease was determined to be medically significant. A copy of the published article is attached as further documentation of the patient's experience.