IRAK1 and colitis: Rb1 and compound K appear to block IRAK-1 and NFκB activation and thereby reduce pro-inflammatory cytokines, IL-1β, TNF-α and IL-6 and cytokine effectors iNOS and Cox-2 in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-treated mice, another model of colitis [59].