NFKB1 and colitis: Regarding the results from in vivo studies, we observed obvious active NF-κb p65 signaling in VitD-deficient and VDR−/− colitis mice compared to wild-type colitis mice, indicating that the suppression of the VitD/VDR pathway stimulated the overactivation of NF-κb p65 signaling in the challenge of DSS.