TACR3 encodes tachykinin receptor 3 (NK3R), a G protein-coupled receptor that binds neurokinin B with highest affinity, and also responds to substance K and substance P. Neuromedin-K binding activates phospholipase C signaling via G(q) protein and increases intracellular cyclic AMP through adenylate cyclase activation. Beyond its well-characterized role in reproduction, TACR3 is widely expressed in the nervous system and contributes to mood disorders, chr4 pain, learning and memory deficiencies, Alzheimer's disease, Parkinson's disease, addiction, hypoxic-ischemic encephalopathy, and schizophrenia 1. Loss-of-function variants in TACR3 cause hypogonadotropic hypogonadism manifesting as pubertal delay, transmitted in autosomal dominant, recessive, or oligogenic patterns 2. TACR3 resides near the top of the hypothalamic-pituitary-gonadal axis and should be screened alongside GNRHR in equivocal pubertal cases 3. Recent evidence suggests TACR3 involvement in hypoxic-ischemic brain damage through alternative splicing mechanisms 4. Multiple neurokinin B receptor antagonists—including fezolinetant, elinzanetant, and pavinetant—are in late-stage development or approved for vasomotor symptoms such as hot flashes 5.