Moreover, that study linkedthe presence of a high CVD risk in the formers with the overexpression of variousprothrombotic and proinflammatory mediators (i.e. PAR-2, TF, MCP-1, or tPA).However, the classical inflammatory cytokines (ie, IFNγ, TNFα,IL-1β, IL-6) that orchestrate common pathophysiological processes in SLE(ie, nephritis, skin manifestations, neurological affectations, etc) were morespecifically linked to aPL-(−) SLE patients, suggesting molecular andcellular specificity of the CV comorbidity. This evidence concerns the gene CCL2 and nephritis.