Strict regulation of its distribution in embryos is the key to normal morphogenesis.2 As a member of RA metabolic enzyme family, CYP26A1 has been confirmed to participate in protecting the development of certain embryonic tissues from inappropriate RA signalling.3Cyp26A1 knockout mice die during mid‐late gestation and display major morphogenetic defects, such as spina bifida, caudal and lumbosacral region truncation.4 CYP26A1 also has been confirmed that play pivotal roles in embryo implantation. This evidence concerns the gene CYP26A1 and spina bifida.