The study conducted by Mingxia Zhou et al. [46] used in vitro experiments to demonstrate that lipopolysaccharide (LPS) suppresses autophagy in colitis through the TLR4-MyD88-MAPK pathway, thereby orchestrating downstream NF-κB activation and resulting in the generation of proinflammatory cytokines and oxidative stress. This evidence concerns the gene NFKB1 and colitis.