These accumulated inflammatory cells can initiate pathological cascades of AMD in several alternative ways: 1) elicit innate immune responses, such as complement and inflammasome activation; 2) produce pro-inflammatory cytokines, such as TNF-α and interleukin-1β; and 3) increase inflammatory cell debris, lipid deposition and oxidative stress. The gene discussed is TNF; the disease is age-related macular degeneration.