In models of autoimmune and inflammatory diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus, inflammatory bowel disease (IBD), and multiple sclerosis, IMPs are markedly upregulated and have been shown to promote inflammation through activation of NLRP3 inflammasomes [93,94], amplifying the production of pro-inflammatory cytokines (e.g., IL-6, IL-17, TNFα), supporting the differentiation of pathogenic Th1 and Th17 cells, and sustaining pro-inflammatory M1 macrophage polarization [35,61,78]. The gene discussed is IL17A; the disease is rheumatoid arthritis.