Collectively, our findings revealed that Dok3 plays a critical role in the negative regulation of TLR4-MyD88-JAK2-STAT3 axis in neutrophils during SARS-CoV-2 infection for the suppression of calprotectin production, and the increased Dok3 levels detected in neutrophils of severe COVID-19 patients (17) could be a compensatory mechanism to blunt elevated calprotectin levels. The gene discussed is STAT3; the disease is COVID-19.