THRA (thyroid hormone receptor alpha) is a ligand-dependent transcription factor that mediates cellular effects of thyroid hormones through heterodimerization with retinoid X receptor and binding to thyroid hormone response elements 1. While THRA can bind thyroid hormone, it functions as a weak dominant negative inhibitor of thyroid hormone action [UniProt]. THRA and THRB have distinct, non-overlapping physiological functions 2. THRA is expressed during early nervous system development 3 and regulates spatiotemporal responses in skin wound healing through phase-coupled mechanisms: epidermal THRA activates glutathione metabolism to accelerate reepithelialization, while dermal THRA mediates extracellular matrix maturation 4. Mutations in THRA cause resistance to thyroid hormone alpha (RTHα), characterized by abnormalities in growth and gastrointestinal function with minimal effects on the hypothalamic-pituitary-thyroid axis, contrasting with RTHβ 2. THRA is predominantly expressed in tissues including heart and bone, where selective THRB activation is preferred therapeutically to avoid THRA-mediated side effects 5. Genome-wide analysis identified THRA as a potential therapeutic target for migraine treatment 6.