Atopic dermatitis (AD) is an autoimmune inflammatory disease, characterized by xerosis, eczematous lesions, redness, persistent, and severe pruritus. In this case report, we show a different option of treatment for severe, chronic refractory cases. 2 | CASE REPORT A 63-year-old man, with a chronic history of severe AD (defined as >10% body surface area involvement and scoring of AD, SCORAD > 20), who had failed multiple systemic therapy. He presented with a history of atopic dermatitis since childhood, which got worse in the past 8 years, increasingly progression with whole body involvement. SCORAD-66.7% DLQI-22 (Figure 1). Previous treatments included topical corticosteroids, tacrolimus ointment, moisturizers, systemic therapy with oral prednisone (1mg/kg/daily) and methotrexate, azathioprine, cyclosporine, antihistamines, antidepressants, thalidomide, and phototherapy, all of them with little or no response. His last attempt was with ustekinumab; however, after 6 months it had no improvement. The patient had a family history of inflammatory bowel disease but denied other autoimmune conditions. Complete review of systems was negative. Physical examination revealed reddish, lichenified plaques involving face, trunk, and extremities affecting approximately 25% of total body surface area (Figures 2 and 3). Given the severity of the disease, the limited and inadequate treatment options, with the patient's concern, we decided to treat with tofacitinib citrate by oral route with JAK inhibitors. At this time, dupilumab was not available in Brazil. Tofacitinib citrate 5mg BID was started. During the first month, he was still on prednisone 20 mg/daily but it was weekly decreased from 20mg to 10mg, then to 5mg until it was totally suspended. During this period, no topical corticosteroids were used, only moisturizers. After three months of treatment, he had nearly complete clearance of face, trunk, upper and lower extremities (Figures 4 and 5). SCORAD-10.1% DLQI-3.