Reports have confirmed that in patients with RA, NLRC4 expression was enhanced in monocytes after treatment with lipopolysaccharide and ATP [19]; G > C mutation at rs479333 of NLRC4 plays a beneficial role in the progression of MS and the response after interferon treatment [21]; through Genome-Wide Association Studies (GWAS) and various omics studies, Zeller et al. [22] demonstrated that rs385076 of NLRC4 has a fatal role in regulating the expression and differentiation of NLRC4 by regulating its binding to the transcription factor PU.1 and is related to the activation of IL-18. The gene discussed is SPI1; the disease is rheumatoid arthritis.