I'm hoping it will be based on the current theory driving the underlying pathology of both pain and loudness hyperacusis.
Loudness hyperacusis is thought to originate from synaptopathy of the A1 nerve fibers connecting with the IHC. Although FX-322 is not targeting synapses directly they have said that they have seen "meaningful connections" reestablish with the IHCs. Although for true synaptopthy we might see better results from Hough or Pipeline.
For pain hyperacusis, another forum member explained to me that sometimes when OHC are damaged they begin to leak ATP which affects the A2 fibers that connect to these OHC. It's thought that this ATP stimulates the A2 nerves, which are involved with pain sensations. If you can repair the OHC hopefully the ATP will stop, and the stimulation of the nerve will cease.
I think someone mentioned a while back that a person in the REGAIN trial experienced improvement in both their hyperacusis and tinnitus, so I think there's a good deal to be optimistic about.