SLC52A1 encodes riboflavin transporter 1 (RFVT1), a plasma membrane protein that mediates vitamin B2 (riboflavin) uptake into cells, particularly in placenta and intestine 1. The gene's transcription is regulated by the Sp-1 transcription factor binding to a GC-rich core promoter 1. RFVT1 exhibits cooperative kinetics for riboflavin transport with a K0.5 of 0.86 μM and is inhibited by riboflavin analogs FMN and lumiflavin 2. Beyond basic transport function, SLC52A1 plays a critical cellular homeostasis role. It is a p53 target gene that suppresses cellular senescence through riboflavin uptake-dependent activation of mitochondrial complex II and the electron transport chain 3. This senescence suppression occurs via FAD-dependent demethylation activity of LSD1, which suppresses pro-senescence genes 4. SLC52A1 mutations cause riboflavin transporter deficiency, an autosomal dominant metabolic disorder with heterogeneous presentations ranging from neonatal multiple acyl-CoA dehydrogenase deficiency-like phenotypes to adult-onset seizures and mild hyperammonemia 5. Intronic variants can cause exon skipping and transient MADD 6. Additionally, SLC52A1 variants are associated with increased risk of early multiple-organ failure in acute pancreatitis 7. The gene represents a key hub integrating riboflavin metabolism with both mitochondrial function and senescence regulation 8.