Given that AXL was not co-expressed with ACE2 or TMPRSS2 in the human lungs or trachea, that downregulation of AXL in ACE2-KO H1299 cells significantly reduced SARS-CoV-2 virus pseudotype infection, and that neither AXL nor ACE2 could block viral infection when the other protein was overexpressed, AXL’s function in mediating SARS-CoV-2 infection is very likely independent of ACE2. The gene discussed is TMPRSS2; the disease is viral infectious disease.