An attempt has been made to evaluate the various cellular effects produced in a bacterial system by the pyrimidine analog, 5-fluorouracil (FU), to determine their interrelationships, and to clarify their role in producing growth inhibition. Several of these drug effects could be dissociated from each other when thymidine (TdR) or combinations of TdR with uracil (U) were added to cultures of Bacillus cereus together with FU. In the presence of TdR, FU still produced inhibition of the increase of cell mass, completely blocked cell division, and produced cell death; while the FU-produced inhibition of DNA synthesis, and the reduction in the number of nuclear areas in the cell was prevented. The biochemical analyses were complemented by microscopic examination. Thus, many of the inhibitory effects of FU on B. cereus, especially those occurring within the first doubling of cell mass after the addition of the analog, are unrelated to the drug’s effect on DNA synthesis. The combination of FU with U and TdR completely prevented all of the inhibitory actions of the analog when added simultaneously. Complete recovery also resulted when U was later added to cultures which had received TdR together with FU to assure DNA synthesis, although normal growth resumed more slowly if the addition of U was delayed. The temporary absence of TdR leading to inhibition of DNA synthesis prevented complete recovery of growth, since the control rate of growth could no longer be attained when the addition of TdR to cultures exposed to FU plus U was delayed. These studies suggest that in addition to its actions on reducing growth as measured by an increase in cell mass, FU inhibited cell division by more than one mechanism. In the absence of sufficient DNA synthesis, replication appeared to be stopped by unbalanced growth and thymine-less death. When DNA synthesis was not deficient, however, FU apparently still interfered with a normal function of U which is required for cell division.