Furthermore, several studies have shown that treatment with the AMPK inhibitor AICAR suppresses RA FLS invasive function [169], decreases spontaneous secretion of proinflammatory mediators IL-6, IL-8, and MCP-1 from ex vivo whole tissue synovial explant cultures, and inhibits the pro-invasive effect of CD4 T on the RA FLS, evident by reduced growth factor and MMPs expression, thus implicating AICAR as potential target for treatment of RA [155]. This evidence concerns the gene CCL2 and rheumatoid arthritis.