To confirm that mTORC1 activity was also required in mice with loss of Tsc2 in rods (rodTsc2−/−) to cause AMD-like pathologies, we generated mice with simultaneous deletion of Tsc2 and the mTORC1 accessory protein Raptor (rodTsc2−/− rodRaptor−/− mice) (Figure 2). This evidence concerns the gene RPTOR and age-related macular degeneration.