Gene expression, the biochemical process by which a cell's genetic code is read out to produce proteins, is a fundamentally stochastic process. One consequence is that even genetically identical populations of cells in homogenous environments can often display significant cell-to-cell variability in the numbers of mRNAs and proteins. This raises a couple of questions. Can cells exploit this randomness in the execution of the genetic code for their own benefit? Conversely, do cells reduce the impact of variability in order to produce reliable outcomes in other contexts? We have developed a method that allows for the detection of individual mRNA molecules in a host of organisms to help us answer these questions by providing us with very sensitive measures of gene expression in individual cells. In particular, we have explored the impact of variability in gene expression on the process of development by studying the gene regulatory network responsible for gut formation during early embryonic development in C. elegans. We found that the normal gut development pathway is remarkably robust, but this robustness can be destroyed by mutations to a single gene that result in wildly varying embryonic fates. We have shown that these different fates result from the variable expression of a key upstream regulator in the rewired mutant gut pathway. These results suggest that redundancy in developmental gene networks can serve to mask and buffer otherwise hidden sources of gene expression variability.