Since considerable evidence shows that MuRF2−/− hearts enhance PPAR-activity suggesting that endogenous cardiac MuRF2 inhibits PPAR activities by nuclear PPRE-binding (Fig. 1a) and PPAR-regulated gene expression (Fig. 4), we next focused on how the muscle-specific ubiquitin ligase MuRF2 might exert its inhibitory effects based on our current knowledge of how ubiquitin regulates PPAR in cancer cells. This evidence concerns the gene TRIM63 and cancer.