Crossing those mice to animals lacking cGAS, IRF3/IRF7, IFN-alpha/beta receptor alpha chain (IFNAR1), adaptive immunity, αβ T cells, and mature B cells, showed that lung disease developed independently of cGAS, IRF3/IRF7, and IFNAR1, suggesting that other triggers than cyclic dinucleotides (the ligands of cGAS) and/or IFN, contribute to STING over-activation within T cells (79). This evidence concerns the gene IFNAR1 and lung disorder.