NFKB1 and colitis: These results strongly suggest that this colitis model is mediated by inflammasome pathway, as previously reported.(26) Further, ketone bodies, which are produced during states of energy deficit like fasting, are reported to block inflammasome-mediated inflammation,(27) and Inflammasome is less activated in fasting humans.(28) In summary, we speculate that activation of inflammasome, but not NF-κB, is the major event of this colitis model, and also a target of fasting therapy.