showed a positive reaction for MPO in neutrophils. Immunostaining for Melan-A revealed no melanoma cells. Gram staining of a biopsy specimen showed a negative result. Laboratory examination revealed hyperneutrophilia (white blood cells, 12000/ll) with differentiation of 87.1% neutrophils, elevated Creactive protein (CRP, 13.14 mg/dl), normal procalcitonin (PCT, 0.09 ng/ml), and normal antinuclear antibody titer (ANA, <1:40). From those clinical and histopathological findings, we diagnosed the patient with vemurafenib-associated neutrophilic panniculitis with vasculitis. Increased dosages of acetaminophen from 1500 mg to 2800 mg and celecoxib from 200 mg to 400 mg were started, and the erythematous lesions improved 10 days after initiation of that therapy without reducing the dose of vemurafenib. Although BRAF inhibitors rarely induce erythema nodosum-like lesions, reported cases histopathologically manifest as panniculitis. Approximately two-thirds of the reported cases with BRAF inhibitor-associated panniculitis had neutrophilic panniculitis. One possible hypothesis about the pathogenesis of neutrophilic vasculitis in BRAF inhibitorassociated panniculitis is that aberrant hyperactivation of the RAF-MEK-ERK signaling pathway in neutrophils activates various functions of neutrophils and results in inflammation. Another possibility is that tumor destruction can cause neutrophilic panniculitis and vasculitis. In our case, small arteries in the subcutaneous adipose tissue were apparently affected, and increased dosages of both acetaminophen and celecoxib dramatically improved the lesions. While the spontaneous disappearance of the panniculitis was described, most of the reported cases required the withdrawal of the vemurafenib. Interestingly, in our patient, the association of acetaminophen and celecoxib led to a rapid healing of the lesions and relieved his discomfort. We considered that the combination of both acetaminophen and NSAIDs such as celecoxib could efficiently suppress the BRAF inhibitor-associated panniculitis. The increased number of melanoma patients treated with BRAF inhibitors will require appropriate assessments and treatments for BRAF inhibitor-associated panniculitis. Efficient control of BRAF inhibitor-associated panniculitis is quite important for the improved management of melanoma patients in the era of molecular-targeted therapies against melanoma.