Of note, although the potential relationship between PPARβ/δ and FOXO1, atrogin-1, and MuRF1 was examined in previous reports [20], [27], [29], the present study is important because it provides novel information about the mechanistic link between PPARβ/δ and sepsis- and glucocorticoid-induced muscle wasting as well as insight into the therapeutic implications of PPARβ/δ inhibition in these conditions. This evidence concerns the gene TRIM63 and Sepsis.