In experimental periodontitis, a chronic infectious and inflammatory disease, and gastrointestinal mucositis, ARBs suppress TNF-α-induced activation of the NF-κβ classical pathway and gene expression of NF-κβ p65 subunit, which induces gene transcription of pro-inflammatory mediators in vascular endothelial cells [43, 45, 46]. This evidence concerns the gene NFKB1 and gastrointestinal mucositis.