Regarding its role in inflammation, there is only one report to date, which showed that overexpression of miR-766 in human rheumatoid arthritis (RA) fibroblast-like synoviocyte MH7A cells stimulated with TNF-a suppressed the expression of various pro-inflammatory genes, such as IL-1β, IL-6, IL-8, and protein of the matrix metalloproteinase (MMP)-3, thus contributing miR-766, in anti-inflammatory responses, through the indirect inhibition of NF-κB signaling [101]. The gene discussed is CXCL8; the disease is rheumatoid arthritis.