ANKRD24 is a structural protein essential for inner ear mechanosensitivity and hearing function. As a component of the stereocilia rootlet, ANKRD24 localizes to the stereocilia insertion point where it forms a ring structure bridging the apical plasma membrane with the lower rootlet 1. ANKRD24 directly organizes and stabilizes TRIOBP-5, an F-actin bundling protein that reinforces the rootlet architecture and maintains proper stereocilia anchoring 1. In concert with taperin (TPRN), which enables F-actin bundling at stereocilia pivot points, ANKRD24 supports optimal mechanotransduction during sound-induced deflections 2. Loss of ANKRD24 function in mice results in progressive hearing loss, TRIOBP-5 mislocalization, diminished auditory recovery after noise exposure, and increased susceptibility to hair bundle overstimulation 1. Clinically, ANKRD24 mutations cause human non-syndromic hearing loss; a homozygous frameshift variant (c.1934_1937del) was identified in an Iranian family with postlingual, moderate-to-severe autosomal recessive sensorineural hearing loss, expanding the genetic spectrum of deafness 3. Beyond auditory function, ANKRD24 participates in ketone body-mediated autophagic clearance of pathological tau in Alzheimer's disease models 4.