Given the proximity of dystrophin to F-actin (which it specifically binds and stabilises) combined with its integral relationship with SRF transcription, we hypothesise that dystrophin loss leads to a shift in actin de-polymerisation, which affects SRF expression and downstream circadian gene expression, thus resulting in circadian dysregulation in DMD models. The gene discussed is SRF; the disease is Duchenne muscular dystrophy.