Accordingly, the IL‐1β–induced PI3K/Akt phosphorylation was inhibited by ATG intervention, which was in agreement with the previous study, showing that pre‐treatment with ATG significantly suppressed PI3K/Akt phosphorylation and NF‐κB activation in LPS‐stimulated peritoneal macrophages and on LPS‐induced systemic inflammation and 2,4,6‐trinitrobenzene sulphonic acid (TNBS)–induced colitis in mice.39 Thus, the inhibitory effects of ATG on NF‐kB activation were followed by inhibition of PI3K/AKT. Here, IL1B is linked to colitis.