SLC25A32 is a mitochondrial inner membrane transporter that facilitates flavin adenine dinucleotide (FAD) and folate translocation into the mitochondrial matrix 1. It provides essential cofactors for flavoenzymes involved in fatty acid β-oxidation, amino acid metabolism, and the glycine cleavage system of one-carbon metabolism 1. The protein is particularly critical for neural tube closure during early embryogenesis through its role in mitochondrial folate metabolism 1. Loss-of-function mutations in SLC25A32 cause folate-resistant neural tube defects in mice that can be rescued by formate supplementation, demonstrating the gene's essential role in embryonic development 1. Biallelic SLC25A32 variants have been identified in human neural tube defect cases 1. Additionally, a SLC25A32 polymorphism (rs2241777) is associated with reduced plasma folate levels and increased fracture risk in postmenopausal women 2. Beyond developmental disorders, SLC25A32 upregulation promotes malignant progression in glioblastoma through PI3K-AKT pathway activation and associates with poorer prognosis 3. The gene also shows differential expression across multiple cancer types with prognostic significance for immunotherapy response 4. Furthermore, SLC25A32 expression is upregulated in psoriatic skin and silica-induced pulmonary fibrosis, suggesting roles in inflammatory and fibrotic disease pathogenesis 5, 6.