Sam68 is required for both TNF and TLR-mediated NF-κB signaling [6, 17], and a number of studies have found it to be a key inflammatory driver in a variety of pathophysiological processes, including chronic auto-inflammatory disorders such as UC [19], arthritis [20], and arterial injury [21] (Fig. 7). The gene discussed is KHDRBS1; the disease is arthritic joint disease.