Dear editor, A 20-year-old female student was admitted to our clinic with a 2-week history of an asymptomatic erythematous plaque on the nasal tip. The lesion arose with no identified causes, including drug use, tattoo, insect bite, and trauma. The lesion showed no change after sun exposure. The patient was otherwise healthy. Previous treatmentwith oral 30 mg prednisone daily had only resulted in temporary relief. Physical examination revealed a 2 cm × 1 cm infiltrative nontender red plaque on the nasal tip (Figure 1a). There were no palpable superficial lymph nodes on the head and neck. Skin biopsy showed a dense lymphohistiocytic infiltration in the superficial and deep perivasculatures and around appendages of the skin (Figure 2). The infiltrate was predominantly composed of CD45RO+, CD3+, CD20+, and CD79a+ lymphocytes. Less than 10% of the infiltrative cells were stained positively for Ki-67. T cell receptor gene rearrangements were negative (Figure 3). The diagnosis of Jessner–Kanof lymphocyte infiltration was made based on clinical manifestations and histological examination. Differential diagnosis included CD4+ primary cutaneous smallto medium-size pleomorphic T cell lymphoma (CD4+ PCSM-TCL) and folliculotropic mycosis fungoides (FMF). CD4+ PCSMTCL mostly affects middle-aged and elderly people. Histopathologically, CD4+ PCSM-TCL is characterized by a predominance of CD4+ pleomorphic T cells. FMF usually presents with pruritic papules. Characteristic histopathologic finding of FMF lesions include variable infiltration of the follicular epithelium by atypical T lymphocytes, which spares the epidermis. The TCR genes of both CD4+ PCSM-TCL and FMF are clonally rearranged. According to the clinical and histopathologic features and the result of TCR rearrangement, PCSM-TCL and FMF were excluded. Other differential diagnosis included discoid lupus erythematosus, syphilid papulosa, nodular skin amyloidosis, which were excluded after serum and pathological assessments. The patient was treated with impulse intralesional injection of compound betamethasone (1 mL, betamethasone dipropionate 6.43 mg equivalent to 5 mg betamethasone, betamethasone sodium phosphate 2.63 mg equivalent to 2 mg betamethasone, DIPROSPAN) once per month. The lesion improved significantly with the first and second course of injection (Figure 1b,c). Marked improvementwas observed 1month after the third injection (Figure 1d). Jessner–Kanof lymphocyte infiltration is a rare, benign, and nonscarring lymphoid proliferation condition. The disease mainly presents with asymptomatic erythematous papules and plaques localized on the head, neck, and upper trunk of middle-aged males. Histologically, it is characterized by perivascular and periadnexal lymphocytic infiltrates of superficial and deep dermis. The disease has a prolonged, recurrent course, which may persist for several months to years. Current options of therapy include thalidomide, antimalarial drugs, interleukin-1 receptor antagonist, topical corticosteroid, and pulsed dye laser, but response is usually unsatisfactory. Given the fact that the disease mainly occurs on the aesthetic regions, such as forehead, face, and neck of adults of reproductive age, as is shown in our case, treatment strategy should be carefully selected to minimize the risk of adverse effects. Impulse intralesional injection delivers therapeutic agent directly into the lesion to maintain a localized and elevated concentration in the tissue, which not only achieve better and prolonged response but also minimizes systemic adverse effects. This therapy has been reported to result in significant improvement of