However, the dose of CDDO-Me may be critical for the treatment of endothelial dysfunction, since a higher concentration of CDDO-Me caused excessive mitochondrial uncoupling [66] and upregulated the expression of the TNFα and monocyte chemotactic protein-1 (MCP-1) mRNAs, resulting in the deterioration of antiatherogenic effects [67]. The gene discussed is TNF; the disease is endothelial dysfunction.