While C. elegans is an animal model of choice to dissect the pathological mechanisms associated with myopathies [58], the antagonisms observed between the GDI1, dystrobrevin and dystrophin orthologues in C. elegans should be confirmed in DMD mammalian models (e.g. the mdx mouse) before considering GDI1 as a promising therapeutic target for DMD. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.