A 76-year-old woman from Veracruz, Mexico, was referred to the ophthalmology clinic for progressive pain and scleral thinning in the right eye (RE). Two months before, an episode of diffuse anterior scleritis was successfully managed with non-steroidal anti-inflammatory drugs (NSAIDs). The patient had bare-sclera pterygium surgery with adjunctive beta-irradiation therapy twelve years ago in the same eye. The past medical history was remarkable for uncontrolled diabetes mellitus (DM; HbA1c=14%). The review of systems was negative for fever, weight loss, and chronic cough. The best-corrected visual acuity was counting fingers at 3 feet in the RE and 20/25 in the left eye. Slit-lamp evaluation of the RE revealed marked ciliary injection, a nasal corneal leucoma, and scleral necrosis at the pterygium excision site (Figure 1A (Fig. 1)). Fundus examination of both eyes showed diffusely scattered microaneurysms and haemorrhages corresponding to a moderate non-proliferative diabetic retinopathy. The fellow eye examination was unremarkable. A work-up was negative for RF, anti-CCP, ANAs, ANCAs against PR3 and MPO. The infectious test included a negative FTA-Abs and a PPD test (8 mm induration; see for a detailed classification of tuberculin skin reactions). Of notice, the patient had the BCG vaccination scar in her right arm. Topical treatment included loteprednol etabonate 0.5% every three hours, besifloxacin 0.6% QID, and aggressive lubrication. Systemic anti-inflammatory therapy consisted of 60 mg of oral prednisone daily, and 15 mg of weekly subcutaneous methotrexate (MTX) combined with an insulin regimen. After one month of therapy, the scleral necrosis progressed, and inflammatory activity was observed at the nasal peripheral cornea (Figure 1B (Fig. 1)). At this point, refractory SISN with peripheral corneal involvement was suspected, and thus, subcutaneous MTX was increased to 25 mg/week, and 1 g of intravenous methylprednisolone was prescribed for three days (Figure 1B (Fig. 1)). Moreover, empirical management with natamycin 5% QID and oral valaciclovir (1 g TID) for fungal and herpetic coverage was initiated. Unfortunately, the scleral necrosis continued progressing (Figure 2A (Fig. 2)); thus, a scleral biopsy, debridement, and a corneal tectonic graft with conjunctival autograft were performed due to impending corneal perforation (Figure 2B (Fig. 2)). Because of severe scleral thinning and a high risk of perforation, tissue sample was insufficient for culture analysis. Smear results, however, came out negative for bacteria, fungi, and mycobacteria. Polymerase chain reaction (PCR) analysis could not be performed due to a lack of insurance coverage. Pathology and smear results of the scarce necrotic tissue came out negative for bacteria, fungi, and mycobacteria. Because of a high risk of perforation, no other tissue was available for histopathologic study. One month later, the corneal tectonic graft lysed completely (Figure 2C (Fig. 2)). At this point, anti-tumor necrosis factor (anti-TNF)-alpha biologic therapy was considered; hence, an interferon-gamma release assay (IGRA) was ordered, resulting positive [Quanti-FERON -TB Gold In-Tube (QFT-GIT) TB1 antigen=1.11 UI/ml]. The chest X-ray, CT-scan, and bronchoalveolar lavage were negative for tubercular disease. Assuming a relationship of the scleral necrosis with active TB infection, antitubercular therapy (ATT) was initiated with a regimen of isoniazid 300 mg, pyrazinamide 1500 mg, ethambutol 1200 mg, and rifampicin 600 mg. The patient continued with topical steroids and antibiotics and a slow taper of oral prednisone for the next two months. The scleral necrosis subsided after one month of treatment. Her fasting glucose level was 117 mg/dl with a regimen of 850 mg daily metformin and 35 U of glargine insulin. An intensive 6-month regimen of ATT with four drugs was planned to reduce isoniazid and rifampicin for the next 6 months. The patient is currently in her seventh month of treatment and an excellent therapeutic response with no pain and no further scleral inflammation or necrosis are observed (Figure 3 (Fig. 3)).