CD4+CTLs may also be involved in AIDs, for example, in patients with systemic lupus erythematosus (SLE), NKG2D+CD4+CTLs expressing GzmB and perforin 1 (PRF1) kill immunoregulatory Tregs in a NKG2D–NKG2DL interaction-dependent (major pathway) and Fas–FasL-dependent manner that aggravates the pro-inflammatory phenotype of the disease [375]. This evidence concerns the gene FAS and AIDS.