Nonetheless, although that muscle catabolic phenotype has been described as a consequence of abnormal insulin metabolism and cytokine mediation [40], none of these metabolic processes were yet defined as modulated in the vascular beds of Gram-negative sepsis; with the exception of selenoprotein P, a protein closely related to insulin metabolism [41], which was significantly downregulated in EC, a fact that has been previously associated with the severity of sepsis and other critical illnesses [42, 43]. The gene discussed is INS; the disease is Sepsis.