Though this conserved function of Vpr modestly impacts cycling CD4+ T-cell infection in cell culture, induction of G2 cell cycle arrest may be so critical to HIV replication in human infection that Vpr-evolved promiscuous use of CRL4-DCAF1 to ensure arrest occurs by whatever means available, regardless of the intracellular environment the virus finds itself in. Here, DCAF1 is linked to infection.