In order to evaluate whether the alteration in LKB1 expression is a downstream consequence of the complex cascade of pathology events occurring in mdx mouse muscles, such as oxidative stress and inflammation, or rather directly related to the primary dystrophin deficiency, we assessed Lkb1 expression in muscle precursors throughout in vitro myogenesis, by RT-PCR analyses using healthy 2B4 (WT) and dystrophic SF1 (DMD) cell lines, as myoblasts or at various time points of differentiation [day (D) 2, D6 and D11] (Fig. 7A). This evidence concerns the gene DMD and Duchenne muscular dystrophy.