Reduced peripheral insulin sensitivity has been suggested as a possible mechanism.22–25 Another possible explanation suggested is beta cell dysfunction, either due to reduced beta cell mass in the pancreas26 or aberrant processing of proinsulin in these cells which leads to relative insulin deficiency.27 A deficient incretin response due to late onset of enteral feeds,28–30 and insufficient control of glucose production are postulated mechanisms as well.31 32 Other perinatal clinical conditions, such as sepsis, might be involved in the pathophysiology of hyperglycaemia.33 The gene discussed is INS; the disease is Sepsis.