SLC16A10 encodes an aromatic amino acid transporter (TAT1) with dual roles in thyroid hormone and amino acid homeostasis 1. The protein mediates sodium- and proton-independent bidirectional transport of thyroid hormones T3 and T4 with high affinity, and low-affinity transport of aromatic amino acids including phenylalanine, tyrosine, tryptophan, and L-dopa 2. SLC16A10 is predominantly expressed in kidney and intestine, where it facilitates aromatic amino acid absorption 2. Clinically, SLC16A10 demonstrates disease relevance across multiple systems. In the auditory system, SLC16A10 deficiency causes hearing loss and cochlear hair cell degeneration, with T3 administration partially restoring function, indicating critical roles in thyroid hormone-dependent cochlear development 3. Recent evidence links SLC16A10 to psoriasis pathogenesis through regulation of arachidonic acid metabolism in keratinocytes; SLC16A10 downregulation alleviates psoriasis severity and hyperinflammation 4. Additionally, SLC16A10 promotes melanogenesis by facilitating phenylalanine uptake, with expression increasing following UVB irradiation 5. SLC16A10 also mediates transplacental transport of liquid crystal monomers, potentially affecting fetal development 6. However, the clinical significance of SLC16A10 polymorphisms in thyroid hormone regulation appears limited; rs17606253 did not significantly affect FT3 levels in athyreotic patients on levothyroxine therapy 7.