Among these genes, CERK, GNL1, PLP1, and MAPK8 are known to be altered or play a direct role in the pathophysiology of IUGR or PE in various pathways discussed above: differentiation and proliferation regulation, response to hypoxia and oxidative stress, and neurological maturation (Vaiman et al., 2011; Reid et al., 2012; Goyal et al., 2013; Chan et al., 2019). This evidence concerns the gene GNL1 and fetal growth restriction.