AIM2 and Sepsis: In addition to well-known PRRs—such as toll-like receptors (TLRs), nucleotide-binding oligomerization domain (NOD)-like receptors, retinoic acid-inducible gene (RIG)-I–like receptors, absent in melanoma 2 (AIM2)-like receptors, C-type lectin receptors (CLRs), and advanced glycosylation end-product specific receptors (AGER/RAGE) [92]—we assume that transmembrane protein 173 (TMEM173; also known as STING), an intracellular immune regulator to PRR activation during infection and tissue injury [93, 94], may be implicated in SARS-CoV-2–mediated sepsis and septic shock.