Although the most dramatic increase in the mass of skeletal muscle occurs after birth, research into skeletal muscle development has tended to focus on the embryo. On p. 601,Klein and colleagues readdress this balance by examining whether adult muscle stem cells recapitulate the mechanisms of embryonic skeletal muscle growth. They focused on the basic helix-group-helix transcription factor myogenin,which is crucial for the development of embryonic skeletal muscle. Surprisingly, they found that conditionally mutant mice that produce no myogenin after late embryogenesis have no consistent muscular abnormalities. At first the authors thought that myogenin might be compensated by other myogenic factors, such as myogenic factor 6, myogenic differentiation 1 and myogenic factor 5. But these proteins were not sufficiently upregulated in the conditional mutants for this to be a plausible explanation. Instead, the authors conclude that adult skeletal muscle development is independent of myogenin, and they speculate on possible roles of the Mef2 proteins, which invertebrates rely on for the development of embryonic muscle.