TEKT3 encodes tektin 3, a microtubule inner protein (MIP) that localizes to the inner lumens of doublet microtubules in ciliary and flagellar axonemes 1. TEKT3 forms filamentous polymers within ciliary and flagellar microtubule walls and interacts with other tektin proteins to form functional complexes 2. The protein is essential for normal sperm motility; TEKT3-null mice produce sperm with reduced motility (47.2% versus control levels) and increased flagellar structural bending defects 3. In humans, bi-allelic TEKT3 mutations cause oligoasthenoteratozoospermia (OAT) characterized by reduced progressive sperm motility and acrosomal hypoplasia, representing a form of male infertility 2. TEKT3 deficiency disrupts axonemal organization, particularly affecting the tektin bundle structure that stabilizes doublet microtubules 4. Clinically, TEKT3 mutations are associated with spermatogenic failure 81 and represent a candidate gene for nonsyndromic asthenozoospermia in humans 3. The protein is enriched in developing spermatids 5 and shows age-related expression changes in spermatozoa from men with declining fertility 6. While TEKT3 deficiency alone permits some fertility in mice, combined knockout with TEKT4 causes subfertility, suggesting partially nonredundant roles 3.