VDR-targeted pathways include TLR, NF-κB signaling, and Th17/Treg cell response: as NFκB-induced pathways are enhanced in VDR-deficient mice exposed to bacterial and chemically-induced colitis, it has been proposed that the anti-inflammatory function of vitamin D depends on the suppression of NFκB activity [132]. The gene discussed is NFKB1; the disease is colitis.