We have previously reported that cardiac specific MuRF2 knockout mice hearts exhibited increased PPAR γ1 protein and deteriorated systolic function in high fat diet induced insulin resistance and cardiomyopathy, indicating the cardioprotection role of MuRF2, and that PPAR γ1 is a potential therapeutic target of diabetic cardiomyopathy; in vitro ubiquitination analyses showed that MuRF2 poly-ubiquitinated PPAR γ1 in a ligand-dependent way and accelerated its proteasomal degradation in HEK293 cells14. Here, TRIM63 is linked to diabetic cardiomyopathy.