Dear Editor, Herein, we report a case of adult T cell leukemia/lymphoma (ATLL) accompanied by toxic epidermal necrolysis (TEN) due to mogamulizumab, a monoclonal antibody targeting the CC chemokine receptor 4. A 74-year-old female with lymphoma-type ATLL was initially treated with CHOP therapy; however, the disease progressed after four cycles of CHOP. She then underwent salvage combinatory chemotherapy with vindesine, etoposide, carboplatin, prednisolone (PSL) (VECP) in combination with a single-dose administration of mogamulizumab (1 mg/kg/cycle) on the first day of each cycle. The initial dose of mogamulizumab was safely administered with no adverse events (AEs), along with conventional methyl-PSL 40 mg, acetaminophen, and dexchlorpheniramine maleate. Thereafter, mogamulizumab was safely administered until the fourth cycle. On day 4 of the fifth cycle of VECP with mogamulizumab, the patient was affected by high-grade fever over 38°C, followed by a focal skin rash on the extremities. Skin biopsy on the next day revealed the pathologic changes consistent with erythema multiforme (EM), which could be an early lesion of TEN or Stevens-Johnson syndrome (Fig. 1a) [1]. Despite the temporal improvement by topical steroid and oral antihistamine, the patient then reported blisters on her soles and oral mucosal erosions on day 10. Then, the dermatitis composed of erythemas, plaques, vesicles, and blisters expanded systemically over 50 % of the body (Fig. 1b, c); the lips and all fingers became swollen (Fig. 1d, e); and her conjunctiva became eros i v e . We d i ag n o s e d he r a s h a v i n g T E N du e t o mogamulizumab treatment and initiated corticosteroid pulse therapy with methyl-PSL 1 g/day from day 11. While the TEN-associated symptoms did not resolve with methyl-PSL pulse therapy alone, the addition of intravenous immunoglobulin (IVIg) led to the improvement of TEN and reepithelialization was observed after 2 weeks. Although mogamulizumab-incorporated immunochemotherapy induced transient stable disease, the patient eventually died of disease progression 4 months after the initiation of mogamulizumab.Sjs has been reported as a life-threatening mucocutaneous AEs during the use of mogamulizumab [2], while the complication of TEN has been rarely reported. The precise etiology underlying TEN has not been fully clarified. However, the association of the deregulated immune reaction, including the impaired Treg function, reactive drug metabolites, and the interaction between the two have been suggested as being causative for TEN [3][4][5]. Although we have unfortunately no data on Treg during mogamulizumab treatment, the impaired Treg function by mogamulizumab could be one of the causatives for TEN in our case [2]. Only a single case of late-onset TEN with mogamulizumab has been reported by Shiratori et al. [6]. Although the duration from the last dose of mogamulizumab to the onset of TEN was different between the case reported by Shirotani and the present case, the clinical course and necessary treatments were similar...