Premature infants born with IUGR are at a several-fold increased risk for mortality and major neonatal morbidities, including RDS, BPD, ROP, and NEC. These severe complications of prematurity are intensified by the effect of suboptimal fetal growth. The possible pathophysiologic processes initiated in utero and continuing after birth have been discussed. Recently reported data suggest that IUGR is a risk factor in programming for the later development of cardiovascular diseases [115-117], hypertension , and diabetes mellitus  in adult life. Experimental research related to the pathophysiology and etiology of these conditions may enable appropriate intervention directed at reducing the excess risk associated with the short- and long-term mortality and morbidity among premature SGA infants.