Macrophages are not permissive to productive SARS-CoV-2 replication in vitro (36, 37), and ACE2-independent macrophage capture of SARS-CoV-2 virus particles by lectins or FcγRs-dependent entry of opsonized virus promotes proinflammatory responses but does not lead to productive viral infection (35, 42–46); furthermore, it triggers inflammatory cell death (pyroptosis mediated by activation of NLRP3 and AIM2 inflammasomes, caspase-1, and gasdermin D). This evidence concerns the gene ACE2 and viral infectious disease.