This is a descriptive study of SCTE, the thrust of which is that SCTE is a form of HAEM that often follows SCT. Clinically, most of the patients with SCTE fell into the EM part of the EM/SJS/TEN spectrum,1- 3 although several exhibited generalized lesions, some of which were confluent. The expression of Pol in a high percentage of the SCTE lesions is consistent with this conclusion. Indeed, Pol antigen was seen in lesional skin from 15 of 19 (79%) of those patients with SCTE studied, a frequency similar to that seen in those with HAEM lesional skin (18 of 24 [75%]), and both were free of infectious virus. These findings, together with the observation that at least 1 patient with SCTE had an increased percentage of circulating CD34+ cells, some of which were also Pol positive, suggest that SCTE behaves like HAEM. However, numerous questions remain. Is the Pol-positive erythematous eruption in patients with SCT caused by the reactivation of a latent HSV infection when acyclovir was discontinued or administered at a low dosage at or after the time of transplantation? Was the SCT an opportunity for more viral DNA fragments to be disseminated peripherally in the circulation? Definitive answers to these questions are not possible at present. Herpes simplex virus reactivation and its processing by the transplanted CD34+ cells is likely because up to 80% of patients undergoing a cancer treatment procedure will have HSV reactivation18 and the percentage of circulating CD34+ cells, which can transport HSV DNA fragments to the skin,15 is markedly increased through the SCT procedure. However, 2 caveats remain. The first is the absence of a detectable, localized HSV-like lesion in patients with SCTE. It is possible that the HSV lesions were hidden (for example, in the nasopharynx) or that they were mild or unnoticed because the patients were intermittently treated with antiviral drugs. The chemotherapeutic agents used for the patients' malignant neoplasms and/or the immunosuppressive drugs prescribed during their illnesses might have dampened the development of clinically visible lesions while allowing for asymptomatic virus shedding, a rather common presentation associated with low virus titers.7,10 The second caveat to the conclusion that SCTE is a form of HAEM is that Pol staining is cytoplasmic, as opposed to HAEM, where it is also intranuclear. The interpretation of this distinct intracellular localization is still unclear. However, staining is specific because (1) skin tissues from healthy subjects and those with DIEM did not stain, (2) staining was not seen in normal perilesional skin, (3) Pol staining was seen in HSV lesional skin from the patient with SCT with generalized HSV that stained with antibody to VP5 and was positive for virus isolation, and (4) normal IgG did not stain. Cytoplasmic localization may reflect deletion of the intranuclear localization signal during DNA fragmentation and/or the loss of a nuclear protein that influences Pol's intranuclear accumulation.19- 21 Patients with SCTE may also represent a distinct EM subgroup and/or distinct Pol-mediated inflammatory responses. It is our belief that SCTE is not restricted to patients with SCT for hematological malignant neoplasms and is likely to also apply to other immunosuppressed transplant patients.