The asexual cell cycle of E. coli produces two genetically identical clones of the parental cell through processive, semiconservative replication of the chromosome. When this process is prematurely disrupted by DNA damage, several recF pathway gene products play critical roles processing the arrested replication fork, allowing it to resume and complete its task. In contrast, when E. coli cultures are starved for thymine, these same gene products play a detrimental role, allowing replication to become unregulated and highly recombinagenic, resulting in lethality after prolonged starvation. Here, I briefly review the experimental observations that suggest how RecF maintains replication in the presence of DNA damage and discuss how this function may relate to the events that lead to a loss of viability during thymine starvation.