During atrophy, Atrogin-1 and MuRF-1 are the crucial muscle-specific ubiquitin ligases that direct the polyubiquitination of proteins to target them for proteolysis by the 26S proteasome [12], shifting gene expression towards a less myogenic phenotype (Atrogin-1, which degrades MyoD) or mediating sarcomeric breakdown (MuRF-1, which degrades myosins) [13], which has vital significance in the research of mechanism of muscular atrophy of cancer cachexia. Here, TRIM63 is linked to cancer.