A number of mechanisms have been proposed to account for insulin resistance in sepsis: suppression of serine phosphorylation resulting from glucocorticoid-induced increases in fatty acids, blockade of PI-3 K pathways by proinflammatory cytokines, and reduction in insulin-facilitated translocation of GLUT-4 in the plasma membrane of cardiac and skeletal muscle caused by activation of adenosine monophosphate-activated protein kinase signaling (Delile et al. 2017; Li and Messina 2009; Vanhorebeek et al. 2005). The gene discussed is INS; the disease is Insulin resistance.