MiR-26b has been associated to RA and inflammation where inhibition of miR-26b in rheumatoid arthritis fibroblast-like synoviocytes (RAFLS) causes increased levels of TNF-α, IL-1β, and IL-6, while miR-26b mimics mediate downregulation of the same proinflammatory cytokines [16]. Here, TNF is linked to rheumatoid arthritis.