All of the aforementioned (and additional) monogenic SLE-like diseases following Mendelian inheritance are usually characterised by disturbed apoptosis, with mutations in the FAS (Fas cell surface death receptor) or FASL (Fas ligand) [42, 43] genes, regulators of activation-induced cell death, resulting in autoimmune lymphoproliferative syndrome (ALPS). This evidence concerns the gene FAS and autoimmune lymphoproliferative syndrome.