The suppression of TH signaling by antithyroid treatment [30]; the inhibition of Dio2 [31,32], the enzyme responsible for converting the prohormone thyroxine (T4) to the active hormone triiodothyronine (T3); the overexpression of Dio3 [32,33], the enzyme responsible for degrading T3; or the deletion of the TH receptor [34] reduces cone degeneration in mouse models of LCA and cone dystrophy/achromatopsia and a chemically induced mouse model of AMD [35,36]. This evidence concerns the gene TH and age-related macular degeneration.