E7 and ARF, like NPM and ARF, display antagonistic properties, but the nucleolar localization of E7 induced by ARF seems to potentiate the enhancing effect of E7 on rDNA transcription. The puzzling idea that a tumor suppressor could exert some Etofibrate oncogenic activity under certain circumstances has always been explored. Troxipide Humbey et al have previously shown that p14ARF may have a tumor �C promoting activity that could limit the progression of some tumors, such as lymphoma. Moreover, McLaughlin-Drubin et al have recently evidenced that p16INK4A, a tumor suppressor highly expressed in response to E7, displays an oncogenic activity in HPV16+ cervical cancer cells depending on inhibition of CDK4/ CDK6 and cellular context. Our results do not prove that p14ARF could exert an oncogenic function by itself. However, it is conceivable that the abundance of each protein may modulate the nature of their cellular partners, as well as their localization and functions. In addition to its negative control of rRNA synthesis, ARF can also inhibit rRNA processing and rRNA nuclear export. These functions can be achieved through ARF binding to NPM and through ARF-induced nucleolar localization of the RNA Pol I transcription termination factor TTF-1. Recently, E7 was shown to upregulate NPM levels in E7expressing differentiating cells and proliferating cells. It is tempting to speculate that this upregulation could contribute to abrogating p14ARF control of ribosome biogenesis. The HPV replicative cycle is unusual. Whereas HPV infects cells of the basal layer of stratified squamous epithelia, new virions can only be produced by differentiated cells of the suprabasal layers which, in physiological conditions, have exited the cell cycle. HPV replication being tightly dependent on cellular DNA replication, the proliferative capacity of infected cells must be uncoupled from their differentiation. Maintenance of S-phase competence in differentiated cells requires the abrogation of cellcycle checkpoints, which is achieved by proteins E6 and E7. Interestingly, however, E6 and E7 expression is only detected in suprabasal layers during the productive viral cycle. ARF is considered to be a potential nucleolar integrator of growth signals, and Apicelli et al recently proposed that basal ARF acts as a monitor of steady-state ribosome biogenesis and growth.