Because enhanced STIM1/Orai1-mediated SOCE is proposed to be an important mechanism of aberrant Ca2+ influx in mdx mice, we evaluated the role of Orai1-dependent Ca2+ entry in the DMD phenotype by crossing mdx mice with muscle-specific, tamoxifen-inducible, Orai1-knockout (Orai1 KO) mice. The gene discussed is STIM1; the disease is Duchenne muscular dystrophy.