The physio-pathological cascade encountered in SLE is a multivalent one, the homeostasis of the internal environment being disturbed on various levels, among which we note the impact of genetic factors such as mutations (protein kinase C delta-PRKCD, Ras, three prime repair exonuclease 1-TREX1, Fas cell surface death receptor-FAS, FAS-ligand, deoxyribonuclease 1), polymorphisms or aneuploidy that can determine family aggregates prone to certain diseases. This evidence concerns the gene TREX1 and systemic lupus erythematosus.