Moreover, mitochondrial damage might play a relevant role in COVID-19 pathogenesis, as SARS-CoV-2 interacts via mitochondrial antiviral signaling protein (MAVS), finally impairing type I interferon production and leading to reduced mitochondrial oxygen sensing, oxidative stress-associated thrombocyte dysfunction, and induction of hemostatic pathways [38]. Here, MAVS is linked to COVID-19.