A woman with no medical history was seen in our department for the first time in 2001 at the age of 62 with erythematous slightly squamous plaques on the right arm and back (Fig 1, A). Skin biopsy was suggestive for sarcoidosis with well-formed noncaseating granulomas. Neither Ziehl Neelsen staining, tissue culture, nor DNA analysis was performed. No systemic involvement was found. From 2001 to 2009, she received successive treatments including hydroxychloroquine, thalidomide, doxycycline, methotrexate, colchicine, and systemic steroids. The lesions failed to respond and were slowly extending centrifugally with atrophic zones, without any systemic involvement (Fig 1, B and C). This treatment failure led to the introduction of adalimumab in 2009. Chest radiograph at this time was normal and QuantiFERON-TB was negative. Adalimumab induced painful ulcerations limited to the plaques that regressed within a few days after stopping the treatment. From 2009 to 2015, she received short courses of oral steroids, dapsone, and doxycycline, without any efficacy. Skin lesions were stable, and there were no symptoms suggestive of internal organ involvement. A new extracutaneous staging was performed in September 2015, including thoraco-abdomino-pelvic computed tomography scan, which was normal, and there was only a slightly high level of serum angiotensin-converting enzyme. Mycophenolate mofetil (MM) was started in November 2015 to treat what was considered to be recalcitrant sarcoidosis. Six months later, the plaques suddenly worsened and became erosive and extensive (Fig 2, A). New extracutaneous staging, including chest radiograph, was normal, and QuantiFERON-TB was negative. A new skin biopsy of ulcerative lesions showed an inflammatory infiltrate in the dermis with an ill-defined noncaseating granuloma (Fig 2, B). Stains for mycobacteria, bacteria, and fungi were negative. The first 24-hour polymerase chain reaction (PCR) (GenoQuick  MTB, Hain Lifescience) was negative. After 5 weeks, tissue culture was positive for a mycobacterium from the tuberculosis complex. DNA analysis by PCR (Genotype MTBC, Hain Lifescience) identified an M bovis that was sensitive to rifampicin, ethambutol, and isoniazid, but resistant to pyrazinamide. MM was discontinued, and a triple therapy comprising isoniazid, rifampicin, and ethambutol was administered for 2 months, followed by isoniazid and rifampicin for 4 months. The ulceration rapidly healed and the lesions gradually resolved and cleared, with only hypertrophic scars remaining at the end of treatment (Fig 2, C) without recurrence after 18 months of follow-up.