Collectively, these actions eventually promote cell fusion by targeting the genes downstream of GCM1, such as syncytins. Furthermore, increased acetylation and desumoylation of GCM1 have been observed in the placentas from pregnancies complicated by IUGR, thus indicating that the posttranslational modification of GCM1 may be involved in the occurrence of fetal IUGR (92). The gene discussed is GCM1; the disease is fetal growth restriction.