This further supports the concept that somatic p53 mutations are one of the etiological factors of RA.94 Nakamachi et al. showed that forced expression of miR-124a in RA-FLSs led to suppression of cell proliferation and G1 phase arrest because miR-124a bound to the 3′-UTR of cyclin-dependent kinase 2 (CDK-2) and monocyte chemoattractant protein 1 (MCP-1) mRNA.95,96 Of note, the expression of miR-124a is dictated by the methylation status of its encoding gene. This evidence concerns the gene CCL2 and rheumatoid arthritis.