A commentary on the above-mentioned study, suggested that the regulation of adiponectin in sepsis may additionally involve the heme oxygenase-1 (HO-1) pathway and its byproduct, carbon monoxide (CO) [58], since studies indicate that CO-releasing molecules can suppress inflammatory cytokine production, modulate metabolism, and influence mitochondrial function, potentially forming an HO-1–adiponectin regulatory axis [59–63]. This evidence concerns the gene ADIPOQ and Sepsis.