Insulin resistance is driven by the stress response to critical illness initiating an overwhelming activation of pro-inflammatory mediators (tumour necrosis factor-α, interleukin-6) and counter-regulatory hormone excess (glucagon, cortisol, catecholamines) which lead to excessive hepatic gluconeogenesis and down-regulation of insulin-mediated GLUT-4 glucose transporters [4]. Here, INS is linked to Insulin resistance.