The finding that dystrophin deficiency leads to constitutive HDAC activation in muscles has provided a rationale for investigating HDAC inhibitors such as givinostat in DMD (Lamb, 2024): given that multiple muscle damage and repair processes are exacerbated by excessive HDAC activity, inhibiting HDAC activity could improve muscle repair and alleviate DMD pathology. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.