Other studies have employed anti-sense morpholino or RNAi knockdowns to show similar dystrophy-like pathology and phenotypes when dystrophin (DMD/BMD), caveolin-3 (LGMD 1C), δ-sarcoglycan (LGMD 2F), or laminin α2 (MDC 1A) proteins are reduced, suggesting that this conservation may extend to other orthologs of human dystrophy-associated genes [10-16]. The gene discussed is DMD; the disease is limb-girdle muscular dystrophy.