Huang et al. [58] performed pharmacological activation of NR1D1 and found that the monomer could directly bind to RORE/RevRE (in a non-NCOR1/HDAC3-dependent manner) to modulate the transcription of nuclear factor erythroid 2-related factor 2 (NRF2) and its downstream antioxidant enzymes superoxide dismutase 1 (SOD1) and catalase, thereby attenuating retinal pigment epithelial and retinal damage and ameliorating oxidative stress in mice with age-related macular degeneration (AMD). Here, HDAC3 is linked to age-related macular degeneration.