The release of inflammatory factors in the tumor microenvironment can activate the NF-κB pathway, which not only directly induces muscle atrophy but also mediates the transcription of atrogin-1 and MuRF-1, leading to increased protein degradation, which indicates that NF-KB is expected to become a therapeutic target for muscular dystrophy [20, 48]. The gene discussed is TRIM63; the disease is muscular dystrophy.