Different stimuli including DNA released by pathogens during infection, leak of nuclear or mitochondrial DNA, or the presence of cyclic di-nucleotides (CDNs) in the cytoplasm lead to the activation of STING, which results in the induction of a signaling cascade and the subsequent transcription of IFNB1 and a multitude of antiviral and proinflammatory genes [1,2]. Here, STING1 is linked to infection.