The replication control genes of bacterial plasmids face selection at two conflicting levels. Plasmid copies that systematically overreplicate relative to their cell mates have a higher chance of fixing in descendant cells, but these cells typically have a lower chance of fixing in the population. Apart from identifying the conflict, this mathematical discussion characterizes the efficiency of the selection levels and suggests how they drive the evolution of kinetic mechanisms. In particular it is hypothesized that: (1) tighter replication control is more vulnerable to selfishness; (2) cis-acting replication activators are relics of a conflict where a plasmid outreplicated its intracellular competitors by monopolizing activators; (3) high-copy plasmids with sloppy replication control arise because intracellular selection favors overreplication, thereby relieving intercellular selection for lower loss rates; (4) the excessive synthesis of cis-acting replication activators and trans-acting inhibitors is the result of an arms race between cis selfishness and trans retaliations; (5) site-specific recombination of plasmid dimers is equivalent to self-policing; and (6) plasmids modify their horizontal transfer to spread without promoting selfishness. It is also discussed how replication control may be subject to a third level of selection acting on the entire population of plasmid-containing cells.