It has recently become clear that the recombinational repair of stalled replication forks is the primary function of homologous recombination systems in bacteria. In spite of the rapid progress in many related lines of inquiry that have converged to support this view, much remains to be done. This review focuses on several key gaps in understanding. Insufficient data currently exists on: (a) the levels and types of DNA damage present as a function of growth conditions, (b) which types of damage and other barriers actually halt replication, (c) the structures of the stalled/collapsed replication forks, (d) the number of recombinational repair paths available and their mechanistic details, (e) the enzymology of some of the key reactions required for repair, (f) the role of certain recombination proteins that have not yet been studied, and (g) the molecular origin of certain in vivo observations associated with recombinational DNA repair during the SOS response. The current status of each of these topics is reviewed.