Cells often rely on precise temporal coordination and can go through great troubles to time events in response to internal signals and environmental cues, as demonstrated by circadian clocks, cell-cycle control, and morphogenesis. But for any given set of signals and cues there can also be substantial random variability from cell to cell. The origin of such variation is understood in general terms—chemical reactions involve random collisions between diffusing molecules—but its extent cannot be inferred from first principles. Most singlecell studies have also focused on fluctuations in molecule numbers (Elowitz et al, 2002; Ozbudak et al, 2002), and there are rather few quantitative measurements (Bean et al, 2006) of intracellular timing even in the best-studied model systems. In this issue of Molecular Systems Biology, Stavans and coworkers (Amir et al, 2007) address this problem in an insightful study of how temporal fluctuations propagate along the lytic cascade of bacteriophage l. When l phage infects a bacterium, it chooses between two paths: it either hijacks cellular resources, overproduces phage particles, and busts the cell open (lysis), or it integrates into the host chromosome and protects the cell from further phage infection (lysogeny). Lysogenic phage then quietly replicates with the chromosome until DNA damage activates the RecA protein, which degrades the l repressor CI and derepresses phage promoters pL and pR. Promoter pL drives the expression of an anti-terminator for pR expression, allowing read-through to lytic downstream genes. A drop in CI thus only triggers lysis if it lasts long enough for pR to remain derepressed by the time the anti-terminator reaches a high enough concentration to allow read-through. This gives the phage a way of jumping ship if the host is in trouble, and gives the cell a grace period in which to repair DNA without a phage mutiny. It also filters out any fast spontaneous stochastic fluctuations in CI concentration that otherwise could trigger lysis without DNA damage. To study this process, Amir et al exposed l-infected Escherichia coli cells to UV light and used fluorescent reporters to measure single-cell response times at different steps in the cascade that leads to lysis. Exposure to high UV led to lysis in