The release of inflammatory factors can activate the NF-κB pathway, suggesting that NF-κB might be a therapeutic target for muscular dystrophy because of the direct induction of muscle atrophy and the transcription of atrogin-1 and MuRF1 for protein degradation, which not only directly induces muscle atrophy but also mediates the transcription of atrogin-1 and MuRF1, leading to increased protein degradation, which indicates that NF-κB is expected to become a therapeutic target for muscular dystrophy [20,28]. This evidence concerns the gene FBXO32 and muscular dystrophy.