Considering the consensus view that assigns a coordinated role for a number of interrelated pathways, i.e., glutamate excitoxicity, oxidative stress, mitochondrial dysfunction, up-regulation of pro-inflammatory mediators, and altered regulation of pro- and anti-apoptotic gene cascades in the injurious processes associated with IH in the CNS [7,38], the protective role of EPO appears to be well justified by the previous evidence indicating that EPO is indeed operative in many of these pathways. Here, EPO is linked to isolated hemihyperplasia.