The very poor pulmonary recovery (about 1% in dog) of 14C-labelled camostat in a distribution experiment [118] poses the legitimate question of whether the pulmonary concentration in therapeutically dosage [109,110,116] is sufficient to generate the TMPRSS2 inhibition demonstrated in vitro [50,119] (i.e., providing prophylaxis of infection) in vivo as well, or whether the anticoagulant and antithrombotic effect of camostat can merely be utilized in SARS-CoV-2 infection/COVID-19. This evidence concerns the gene TMPRSS2 and infection.