Human genetic predisposition (host high-risk Human Leukocyte Antigen haplotypes, higher expression of angiotensin converting enzyme polymorphisms and cellular proteases [e.g. Furin and TMPRSS2 involved in viral entry and infectivity]) can explain why some individuals are severely affected upon infection by SARV-CoV-2 resulting in severe inflammatory lung injury [28–30]. The gene discussed is FURIN; the disease is infection.