Nevertheless, while the exact role of IFN signaling for the pathogenesis of COVID-19 is still controversially discussed and likely depends on the stage of the disease (80–82), our finding that hypoxia specifically enhances chemokine ISG expression in the context of SARS-CoV-2 infection suggests that monocytes within a hypoxemic environment might contribute to the progression from a local inflammatory disease to a systemic inflammatory response syndrome (83–85). This evidence concerns the gene IFNA1 and systemic inflammatory response syndrome.