SLC35F2 is a plasma membrane transporter with dual physiological and pathological roles. Primarily, it functions as a high-affinity importer of queuine (Km 67 nM) and queuosine (Km 174 nM), bacterially-derived micronutrients acquired from the gut microbiome and diet 1. These compounds are incorporated into tRNAs at the wobble position for efficient translation of histidine, tyrosine, aspartate, and asparagine codons 1. The transporter localizes to both plasma membrane and Golgi apparatus and shows high selectivity for queuine/queuosine over other nucleobases 1. In blood-brain barrier models, SLC35F2 facilitates drug transport, particularly in primates, though its relevance varies between species 2. Pathologically, SLC35F2 is significantly upregulated in multiple cancers including pancreatic, thyroid, and hematologic malignancies 34. It promotes cancer progression by inhibiting ferroptosis through the SLC35F2-SYVN1-TRIM59-p53 axis 3 and activating TGFBR1/ASK1/MAPK signaling in thyroid cancer 4. SLC35F2 expression is regulated by βTrCP1-mediated ubiquitination 5 and influences sensitivity to therapeutic agents like YM155 in leukemia cells 67. This positions SLC35F2 as both an essential nutrient transporter and potential cancer therapeutic target.