Gain-of-function mutations of STING (Table 2) have also been linked to the autoimmune disease familial chilblain lupus (FCL) [105, 108], a rare hereditary form of SLE commonly associated with cytoplasmic DNA accumulation in monogenic mutations of exonucleases TREX1 [187, 188] or SAMHD [189] (Figure 5). Here, TREX1 is linked to systemic lupus erythematosus.