To determine whether targeted re-expression of clrn1 in the Müller glia could serve as a therapeutic option for preventing or slowing retinal degeneration in USH3A, we subjected the gfap:Clrn1 transgenic zebrafish to high-intensity light treatment, which was previously established to induce cell death in clrn1−/− zebrafish (Figure 5). The gene discussed is GFAP; the disease is retinal degeneration.