Finally, a recent study on premature infants with encephalopathy occurring in the setting of hypoxia-ischemia, suggested that neonatal brain injury and long-term damage was due to CBS upregulation, highlighting this pathway as a potential molecular target to counteract encephalopathy in premature infants also taking into account that up to 50% of these children showed ASD [125]. The gene discussed is CBS; the disease is Encephalopathy.