In a now classic example of genetic redundancy, overexpression of the basic helix–loop–helix (bHLH) transcription factor MyoD or other members of the MyoD family of myogenic regulatory factors (MRFs) can transform numerous cell types into muscle, but homozygous knockout of either MyoD or other MRFs alone in mice results in fairly normal myogenesis (Weintraub et al. 1989; Braun et al. 1992; Mak et al. 1992; Rudnicki et al. 1992). That no muscle is formed in double mutants (Rudnicki et al. 1993) where the function of two or three MRFs is eliminated (Kassar-Duchossoy et al. 2004) demonstrates that MyoD and other MRFs have overlapping, or redundant, function (Rudnicki et al. 1993; Weintraub 1993). Genes with completely overlapping function cannot be maintained across large evolutionary time, and MyoD and Myf5 knockout mutants do in fact have different, albeit relatively subtle, phenotypes (Kablar et al. 1997; Ordahl and Williams 1998). Weintraub (1993) first suggested that the overlapping function and reciprocal regulation of MyoD and Myf5 result in a genetic circuit with switch-like behavior to irreversibly commit cells to the myogenic pathway. Other transcriptional regulators have also been implicated in vertebrate myogenesis, in particular, the additional MRFs and members of the MADS/MEF2 family, and with their characterization the model of a highly cooperative network controlling muscle development has been further substantiated (Molkentin and Olson 1996; Yun and Wold 1996). Recent work in the nematode Caenorhabditis elegans (Fukushige et al. 2006) reinforces parallels between vertebrate and invertebrate myogenesis, demonstrating conservation of regulators and redundancy, while resolving a long-standing paradox between vertebrate and invertebrate myogenesis. The essential role of vertebrate bHLH MRFs in myogenesis led to surprise when it was found in both the nematode C. elegans and the fruitfly Drosophila melanogaster that the single MyoD homolog (hlh-1 and nautilus, respectively) is not required for muscle specification (Paterson et al. 1991; Chen et al. 1992). A study by Fukushige et al. (2006) in this issue of Genes & Development conclusively demonstrates that hlh-1 does control muscle specification in C. elegans, but as shown previously, its function is masked by genetic redundancy (Baugh et al. 2005b). Fukushige et al. (2006) corroborate and extend previous results (Baugh et al. 2005a,b) demonstrating that hlh-1 (CeMyoD), unc-120 (MADS-box/ SRF), and hnd-1 (HAND/bHLH) redundantly control muscle specification in C. elegans. Together these three genes comprise a functionally robust “muscle module” with implications for the evolution of contractile cell types as well as the dynamics and robustness of muscle cell fate specification. In particular, the closest vertebrate homologs of unc-120 and hnd-1 (SRF and HAND) play prominent roles regulating smooth and cardiac muscle development but not skeletal, which is homologous to the body wall muscle of C. elegans. The fact that all three factors are found to coordinately regulate body wall muscle development led Fukushige et al. (2006) to suggest a common evolutionary origin for all muscle followed by divergence, rather than multiple, independent origins of muscle (see Fig. 1). Furthermore, evolution has favored overlapping function and reciprocal regulation among multiple myogenic regulators, along with the regulators themselves. We thus extend their suggestion and propose that such a redundant, modular network controlling myogenesis allows for dynamic compensation of function, rendering muscle development robust and perhaps even enabling evolution of different types of muscle.