In patients with colitis, the binding of inflammatory factors to the receptor by intestinal mucosal tissue cells activates IκB kinase through the upstream PI3K/AKT signaling pathway, prompting serine phosphorylation of the phosphorylation site of the NF-κB·IκB complex, which in turn leads to ubiquitinyl modification and promotes the release of large quantities of NF-κB in patients [35, 36]. Here, AKT1 is linked to colitis.