In the highly active antiretroviral therapy (HAART) era, the incidence of many cancers remains higher in the HIV-positive than in the general population. This is not only true for AIDS-defining malignancies, such as Kaposi's sarcoma or lymphoma, but also for other cancers, which comprise 58% of all neoplasms in a recently described US cohort [1]. This trend has generated renewed interest in understanding the molecular mechanisms of carcinogenesis in the immune suppressed patient. Potential explanations include prolonged survival of patients with HIV on HAART, high incidence of co-infection with oncogenic viruses, and exposure to risks such as smoking and alcohol [2].