To further dissect possible mechanisms downstream of mTORC1 that contribute to disease progression in our mouse model, we generated mice with simultaneous deletion of Hk2 and Tsc2. This corrected the increase in retinal lactate levels seen after constitutive activation of mTORC1; however, it did not prevent the occurrence of AMD-like pathologies. This evidence concerns the gene HK2 and age-related macular degeneration.