In the early stage of AD, the autophagy level of neuronal cells is gradually enhanced, which helps to remove damaged organelles, misfolded proteins and harmful factors, such as IL-1β, L-6, TNF-α, etc. Nevertheless, with the accumulation of abnormal substances, the autophagy-lysosome pathway is gradually blocked, concomitant with the enhanced LC3-II, and impaired binding of autophagosomes to lysosomes, which in turn promotes the development of AD (Switon et al., 2017). The gene discussed is TNF; the disease is Alzheimer disease.