NFKB1 and colitis: Although we have shown that a possible mechanism of inhibition of the anti-inflammatory activity of caulerpin would be through inhibition of the signaling pathway of NFκB, which is a potent pro-inflammatory signaling pathway, we do not deny the possibility of CLP acting through other pathways, such as inhibiting the pathway of MAP kinases [41], through antioxidant activity [20] or increasing A2AR expression [31], and this last pathway plays an important role in the colitis [55].