TECTA encodes tectorin alpha, a major non-collagenous component of the tectorial membrane—an extracellular matrix structure in the inner ear that overlies the cochlear neuroepithelium and contacts the stereocilia of sensory hair cells. Sound-induced movement of hair cells relative to the tectorial membrane deflects stereocilia and triggers fluctuations in hair-cell membrane potential, transducing acoustic signals into electrical impulses. Pathogenic variants in TECTA cause autosomal dominant and recessive forms of non-syndromic hearing loss. In Europe, TECTA mutations account for approximately 18% of autosomal dominant non-syndromic hearing impairment cases (DFNA8/12) 1, and are also found in a subset of Menière's disease families 2, 3. Recent studies identify ultrarare TECTA variants in approximately 8.9% of age-related hearing loss cases versus less than 1% of controls, suggesting a role in presbycusis 4. The typical clinical phenotype associated with TECTA variants is slowly progressive, mid-to-high frequency sensorineural hearing loss, often beginning in childhood and responsive to hearing aid amplification 5. At the population level, gnomAD v4.1 classifies this gene as loss-of-function tolerant (LOEUF=0.66); this is distinct from the clinical pathogenicity demonstrated by 123 ClinVar pathogenic or likely pathogenic variants documented in disease contexts.