The pathophysiological mechanisms that explain the hypoglycemic syndrome are glucose consumption by the tumor and excess secretion of insulin‐like growth factor II (IGF‐II), a protein that inhibits the release of glucose by the liver, and substances that inhibit its action or the secretion of counterinsular hormones, which lead to the failure of one of the mechanisms to prevent hypoglycemia.1 This evidence concerns the gene IGF2 and neoplasm.