Because previous studies suggest a special contribution of HDAC2 in the pathogenesis of DMD (Colussi et al., 2008; Cacchiarelli et al., 2010) and S1P directly binds and inhibits HDAC2 (Hait et al., 2009), it is tempting to suggest that S1P exerts its beneficial effects on dystrophic muscles by inhibiting HDAC2 activity, thereby relieving ‘beneficial genes’ (HDAC2 target genes) from repressed states. Here, MBTPS1 is linked to Duchenne muscular dystrophy.