It is important to note that other studies in animal models have shown that activation of the TLR4/MyD88/NF-κB axis can induce significant cardiac inflammation in conditions such as acute myocardial infarction or post-traumatic stress [34,35], but these models differ from the post-infectious context without active viral replication that characterizes the SARS-CoV-2 infection model. This evidence concerns the gene NFKB1 and acute myocardial infarction.