The mechanisms of endothelial dysfunction in SLE patients may be upregulated expression of ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1), increased secretion of chemokines such as MCP-1, IL-6, IL-17A, and TNF-α, and the promotion of the activation of the transcription factor NF-κB p65 in human endothelial cells by immune complexes (Gómez-Guzmán et al., 2014; Tan et al., 2014). The gene discussed is CCL2; the disease is systemic lupus erythematosus.