Based on several existing mechanistic studies, we speculate that ATG16L2 might strengthen autophagy in patients with AD, while the latter inhibits the abnormal accumulation of Aβ and causes a simultaneous decrease in the proinflammatory factor NOD-like receptor pyrin 3 (NLRP3) (Bai and Zhang, 2021). The gene discussed is ATG16L2; the disease is Alzheimer disease.