Increased apoptosis, impaired clearance of apoptotic cells, impaired immune regulatory functions with consequent lower activation thresholds of T and B lymphocytes, reactive antibodies against intracellular constituents of nucleosomal DNA proteins and ribonucleoproteins, and dysregulation of the cytokine network, particularly the overexpression of TNF-α and type 1 interferons, all together drive the inflammatory process causing the tissue damage in lupus erythematosus [27, 28, 45]. This evidence concerns the gene TNF and lupus erythematosus.