The patient, a 47-year-old white man, had sudden onset of scalp irritation, redness, and itching with rapid hair loss. Although he had long-standing male-pattern hair loss with thinning hair on the top of the scalp, he observed new hair loss involving the entire scalp. The patient had no other significant medical problems; he was taking finasteride, 1 mg/d orally. On examination, he had frontal and vertex pattern hair loss with miniaturization. Along the temporal and occipital rim he had scattered areas of patchy hair loss 1 to 2 cm in diameter, with absence of follicular markings (Figure 1A). At the active border of the patches, there was perifollicular scaling and erythema. A pull test was positive for anagen hair. A scalp biopsy specimen showed decreased numbers of anagen follicles, a dense perifollicular lymphocytic infiltrate at the level of the isthmus, and decreased sebaceous glands (Figure 2A), confirming a histologic diagnosis of lymphocytic PCA, and consistent with the clinical findings of LPP. At the initial evaluation, the severity of his disease was scored using a previously described cicatricial alopecia flowchart that records 3 main end points at each patient visit: severity of symptoms; clinical disease activity, including the anagen positive pull test; and progression of hair loss.1 Treatment regimens over the subsequent 1.5 years included oral prednisone, hydroxychloroquine sulfate, 200 mg twice daily, oral antibiotics (doxycycline hyclate, 100 mg twice daily), mycophenolate mofetil hydrochloride, 1 g twice daily, intralesional corticosteroid injections, high-potency topical corticosteroid solution and shampoo, topical tacrolimus, and antiseborrheic shampoo (ketoconazole). The patient declined a trial of oral cyclosporine because of concerns of adverse effects. Although he experienced some improvement in clinical symptoms and clinical signs, his scalp itching persisted, as did his perifollicular scaling and erythema. A scalp biopsy specimen taken after treatment showed a decreased but persistent inflammatory infiltrate (Figure 2B).