MYO15A, an important gene, is the third most crucial one in hereditary sensorineural hearing loss after GJB2 and SLC26A4 [2]. It is widely recognized as a cause of autosomal recessive non - syndromic sensorineural hearing loss (NSHL) globally. Although its exact function within biological pathways is not elaborated in the provided references, its significance in auditory function is clear from its association with hearing loss. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, could potentially be valuable in further elucidating its functions.

Mutations in MYO15A accounted for 3.58% (81/2263) of all NSHL cases in a Chinese study. The detected variants included missense, frameshift, nonsense, splice site, in - frame, non - coding, and synonymous types, with missense being the most common. Cases with MYO15A variants mostly showed early - onset, symmetric, severe - to - profound hearing loss. The biallelic non - truncating MYO15A variants commonly caused profound HL, and cases with one or two truncating MYO15A variants tended to increase the risk of HL [1]. A meta - analysis showed that the pooled frequency of MYO15A mutations between patients suffering from ARNSHL was 6.2% (95% CI: 4.9 - 7.8, P - value < 0.001), indicating its significant contribution to hearing loss in many countries [2].

In conclusion, MYO15A is a major gene responsible for NSHL. The study of MYO15A through model - based research, especially KO/CKO mouse models, could potentially further clarify its role in auditory function and the mechanisms underlying hearing loss, providing insights for understanding the disease and potentially developing treatment strategies.