Type I interferons, including INF-γ and INF-α, have been used for several years to inhibit NLRP3 and other inflammatory bodies in various autoimmune and autoinflammatory diseases, and INF-γ was significantly upregulated in ulcerative colitis (p < 0.001) to activate the NLRP3 inflammasome, which promotes inflammation. The gene discussed is IFNA17; the disease is ulcerative colitis.