Treatment of emerin-null cells with theophylline, an HDAC3-specific activator, improves myotube formation, whereas the addition of the HDAC3-specific inhibitor RGFP966 blocks myotube formation in wild-type and emerin-null myogenic progenitors (Collins et al., 2017), suggesting that the altered interaction between emerin and HDAC3 is important in the EDMD disease mechanism. The gene discussed is HDAC3; the disease is Emery-Dreifuss muscular dystrophy.