A few constraints should be noted: (1) Even though joint activation of HRI and GCN2 on eIF2α leads to ATF4 and VEGFA promoting cell growth in retinal endothelial cells, other unknown factors might also play a role; (2) How well this pathway applies to real-world AMD cases or other blood vessel diseases needs further confirmation; (3) The exact way HRI and GCN2 interact at the phosphorylation level is still unclear. The gene discussed is EIF2A; the disease is age-related macular degeneration.