However, in parallel to the up-regulation of GAD67 in the contralateral cortex due to treatment with AMD3100, we also observed significantly higher levels of GAD65 in the contralateral cortex of AMD-treated mice (1.27 ± 0.09, n = 6) compared to vehicle-treated mice (0.79 ± 0.12, n = 5) after PT (Fig. 6C). The gene discussed is GAD2; the disease is age-related macular degeneration.