Because it is widely believed that cutaneous CMV disease arises from reactivation of a local latent virus or by autoinoculation in periorificial areas by fecal, urinary, or salivary shedding of CMV,10 CMV ulcers limited to unusual sites, such as the trunk, will go unrecognized unless a search is made to identify relevant pathogens. These cases indicate the need for monitoring of CMV reactivation even in immunocompetent patients, particularly when unexplained ulcers suddenly develop in patients with DIHS, and suggest that a high index of suspicion and early intervention may decrease morbidity, as in case 2. These cases raise the question of why CMV ulcers were exclusively located on the trunk and shoulders, where CMV ulcers are rarely seen, but not in the anogenital sites. Although comprehensive explanations are unavailable, we suggest the presence of unrelated preexisting factors that contribute to CMV reactivation in these lesions, which may increase the risk of ulceration. In view of the previous observations that anogenital ulcers frequently develop after erosive lesions associated with herpes simplex virus infection in human immunodeficiency virus–infected patients,16 a preceding herpesvirus reactivation may play a pivotal role in CMV reactivation. Given the potential interaction of HHV-6 with other herpesviruses in DIHS and the ability to activate Epstein-Barr virus, CMV, and human papillomavirus,17,18 it is attractive to suppose that the preceding HHV-6 reactivation may have induced CMV reactivation, with the result of the sequential development of CMV ulcers at a particular anatomical location. Indeed, the present sequential analyses of patients with DIHS by means of real-time PCR revealed a good correlation between the degree of preceding HHV-6 DNAemia and a clinically significant CMV reactivation as evidenced by CMV antigenemia or a dramatic increase in leukocyte CMV loads. Other studies19 in the setting of bone marrow transplantation also demonstrated that CMV reactivation is consistently preceded by HHV-6 reactivation. If so, patients with DIHS, in which HHV-6 reactivation is commonly seen, would be at risk for subsequent CMV disease.