TMPRSS2 and viral infectious disease: From the perspective of a possible role in viral infections, it is notable that although HAT/TMPRSS11D had been implicated as a possible facilitator for the original SARS-CoV pathogen [155,157], its capacity to serve in a manner analogous to TMPRSS2 in the cleavage of the SARS-CoV-2 Spike protein and subsequent host-cell induction is measurably diminished by a factor of roughly 19-fold [158].