Although numerous reports showed that increased expression and activity of the ubiquitin-proteasome proteolytic pathway, including a dramatic upregulation of the muscle-specific ubiquitin ligases atrogin-1 and MuRF1, play an essential role in sepsis-induced muscle wasting [42, 43], the present study did provide evidence that activation of the calpain system is an additional important mechanism of burn-induced muscle wasting. This evidence concerns the gene TRIM63 and Sepsis.