This new trial is a real breakthrough, demonstrating that you can restore the functionality of a defective gene in the inner ear, opening the way to a host of new treatments. One important caveat is that the gene must also still be relevant post-development of the cochlea (i.e., in children and even adults), and that the extent of gene replacement is sufficient. Those questions can be addressed in mouse models (“knock-out” mice that carry an artificial gene deletion).
The problem with age-related hearing loss without a clear genetic cause (a huge market!) is, first, that there seem to be no good candidate genes whose overexpression might do the job. Second, no good mouse models (these animals live only for two years or so).
Such a therapy might nevertheless come for acute noise-induced hearing damage (good mouse models there), which bears some similarity to age-related hearing loss (both affecting sensorineural cells).