Duchenne muscular dystrophy – a lethal disease caused by dystrophin mutations – is characterised by age-dependent muscle wasting. Mario Pantoja and co-workers now report that increased intracellular sphingosine 1-phosphate (S1P) suppresses dystrophic muscle phenotypes in a Drosophila Dystrophin mutant (see p. 136). The researchers use localisation of Projectin protein (a titin homolog) in sarcomeres, as well as muscle morphology and movement assays, to show that reduction of wunen (a homolog of lipid phosphate phosphatase 3, which dephosphorylates several phospholipids in higher animals) suppresses dystrophic muscle defects; wunen is known to suppress a wing vein defect also seen in Drosophila Dystrophin mutants. Hypothesising that wunen-based suppression may be through elevation of S1P, which promotes cell proliferation and differentiation in muscle, the researchers use several genetic approaches and pharmacological agents to raise S1P levels in the dystrophic flies. In each case, increased S1P levels suppress dystrophic muscle phenotypes. The researchers suggest, therefore, that Drosophila could be used to identify small molecules that might suppress muscle wasting in human patients.