We, therefore, investigated whether the upregulation of neutrophil adhesion molecules, such as integrin receptor Mac-1 (αMβ2; CD11b/CD18), PSGL-1 (CD162), or CAECAM8 (CD66b), could have mediated PNC formation in response to SARS-CoV-2 infection at early stages of mild-to-moderate COVID-19. The gene discussed is SELPLG; the disease is COVID-19.