Multiple studies have already examined this relationship at the bulk level.[20, 21] IL1β and TNF-α are key mediators of host immunity during pathogen infection and other inflammatory conditions.[22] Prescription drugs targeting both IL1β and TNF-α have been demonstrated as effective tools for the remediation of pain and symptoms in a wide range of chronic inflammatory diseases such as rheumatoid arthritis[22–25], gout[22], diabetes[22, 26, 27], and Crohn’s disease[28]. The gene discussed is IL1B; the disease is gout.