Abstract: Fetal growth restriction(FGR) is a common pregnancy complication that is closely associated with adverse outcomes, such as high perinatal mortality, adolescents' major health problems, and chronic adulthood diseases(e.g., cardiovascular and metabolic diseases). Although FGR affects up to 5% to 10% of pregnancies worldwide, there is currently no reliable and effective prevention and treatment method. Vitamin D is one of the fat-soluble hormones pivotal for body health. In addition, 1,25(OH)₂D, which is biologically an active form of vitamin D, exerts a broad range of biological functions by specifically binding to vitamin D receptor(VDR), playing an important role in the maintenance of normal pregnancy, as well as the growth and development of the fetus. Moreover, VDR is a member of the nuclear superfamily receptor, as well as being an important component of the vitamin D metabolic pathway. VDR also mediates virtually all of the known biological actions of the hormonal ligand 1,25-dihydroxyvitamin D₃[1,25(OH)₂D₃]. These actions are directed toward the nucleus, where the VDR binds to the regulatory regions of target genes, and modulates their transcriptional output. The polymorphisms of the VDR are associated with the genetic susceptibility of various diseases by affecting the transcriptional activity of VDR, altering the function of VDR protein, and directly or indirectly influencing the functions of vitamin D. Evidences of human and animal studies have shown that VDR is expressed in endometrial stroma and early decidual cells, VDR proteins are involved in the immune regulation of early embryo implantation, and VDR expression is decreased in the placenta of FGR patients. Therefore, the status of vitamin D and VDR gene polymorphism during pregnancy may be associated with FGR and low-birth-weight newborns. This article reviews the relationship among vitamin D, VDR gene polymorphism, and FGR.