ORAI1 and Duchenne muscular dystrophy: Subsequent studies found that increased STIM1/ORAI1-dependent SOCE also contributes to the enhanced Ca2+ influx observed in DMD (Figure 1), as both the expression and activity of STIM1/ORAI1-mediated SOCE are markedly enhanced in mouse models of MD [59,60] and the dystrophic phenotype of mdx is reduced by inhibiting Orai1-dependent SOCE [101].