All of these changes result in a stimulating inflammatory response by increasing tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), leading to an abnormal placental vascularization (and in some cases to a placental insufficiency with intrauterine growth restriction), multiorganic endothelial dysfunction, and development of clinical features [2,6,7,8]. The gene discussed is IL6; the disease is fetal growth restriction.