Since STING/IRF3-dependent IFN production by macrophages has been reported as a key driver of severe ANCA-associated vasculitis leading to endothelial damage, pulmonary hemorrhages, and lung dysfunction (Kessler et al., 2022), we sought to determine the impact of SAVI immune cells in further promoting endothelial activation and inflammation. The gene discussed is IFNA1; the disease is anti-neutrophil cytoplasmic antibody-associated vasculitis.