TLR4 and atherosclerosis: Indeed, in atherosclerosis, diverse proinflammatory pathways are hyperactivated (e.g., TLR4/NF-κβ) and cytokines are chronically overexpressed (28), which may amplify the immune-mediated response to the SARS-CoV-2, increasing the susceptibility to a cytokine storm, and plaque rupture and thrombosis.