The disrupted Th17/Treg balance caused by aberrant miR-20a expression was suggested to be closely related to the activation of the NLRP3 inflammasome.166 MiR-21 deficiency in RA patients promotes the pathogenicity of Th17 cells via potent STAT3 expression and mediates Treg dysfunction via reduced FoxP3 levels.153 Jin et al. identified Maresin 1 (MaR1) as a mediator upstream of miR-21 that upregulates its expression. The gene discussed is FOXP3; the disease is rheumatoid arthritis.