Computational approaches implemented by us and others [5] have been applied to unravel the driving forces, on an atomic level, of the dominating mutations for SARS-CoV-2 variants that stabilize the S-protein RBD-ACE2 complex; and that can potentially retard hydrolysis of the furin cleavage site and enhance viral infection and transmissibility. This evidence concerns the gene ACE2 and viral infectious disease.