Moreover, the onset time of jaundice in G6PD-deficient newborns is delayed compared to the other CHAs, with a bilirubin peak in the 2°–3° day of life, making G6PD deficiency jaundice hardly distinguishable from the physiological one [26,27,28] In contrast, the most severe cases of CHAs may manifest early in fetal life, with intrauterine growth retardation (IUGR) and nonimmune hydrops fetalis syndrome, requiring in utero transfusions, which may lead to premature birth or even death [16,29,30,31]. Here, G6PD is linked to fetal growth restriction.