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Skeletal muscle tissue is composed of multinucleated fi bers that arise at defi ned periods of embryogenesis from fusion of myoblasts (Buckingham et al., 2003). In particular, embryonic and fetal myoblasts, originating from different waves of myoblasts (Cusella-De Angelis et al., 1994; Relaix et al., 2005), give rise to primary (at about embryonic day [E] 11–12) and secondary (at about E15–16) fi bers, respectively (Ontell and Kozeka, 1984). Subsequently, muscle masses undergo extensive growth in the fetal and postnatal period, and this growth is supported by specialized cells, the satellite cells, situated within a niche between the plasmalemma and the basal lamina of fi bers (Tajbakhsh, 2003). Throughout myogenesis, a fi ne balance among proliferation, differentiation, and fusion is required for the correct formation of the defi nitive muscle units (Tatsumi et al., 2002; Buckingham et al., 2003). Many positive and negative signals responsible for the regulation of such a fi ne balance have been identifi ed, acting at both embryo/fetal stages and postnatally. These include transcription factors, such as MyoD, Myf5, MRF4, and myogenin, as well as extracellular agonists and antagonists, such as members of the insulin-like growth factor (IGF) and TGFβ families, FGF, hepatocyte growth factor, and bone morphogenetic protein (BMP) and its antagonists follistatin and chordin (Balemans and Van Hul, 2002; Parker et al., 2003). <doi>10.1083/jcb.200507083</doi><aid>200507083</aid>Follistatin induction by nitric oxide through cyclic GMP: a tightly regulated signaling pathway that controls myoblast fusion