The molecular control of gene expression in development is mediated through the activity of embryonic enhancer cis-regulatory modules. This activity is determined by the combination of repressor and activator transcription factors that bind at specific DNA sequences in the enhancer. A proposed mechanism to ensure a high fidelity of transcriptional output is functional redundancy between closely spaced binding sites within an enhancer. Here I show that at the bithorax complex in Drosophila there is selective redundancy for both repressor and activator factor binding sites in vivo. The absence of compensatory binding sites is responsible for two rare gain-of-function mutations in the complex.