We disagree with these conclusions, however, for the following reasons: First, the bradykinin storm hypothesis could explain some of the pulmonary manifestations but the same pathological model does not explain other extrapulmonary effects of COVID-19, such as myocardial, renal and central nervous system disease manifestations. In fact, most translational medicine research suggests organo-protective effects of bradykinin especially via B2 receptor [5]. Second, if bradykinin is assumed to be the key inflammatory mediator, bradykinin-mediated nasal congestion, sneezing, rhinorrhoea and sinusitis as seen in common viral rhinitis [6], should be common symptoms of COVID-19 diseases and pulmonary manifestations like wheezing and bronchospasm should be profound. On the contrary, only ~ 4% of COVID-19 patients complain of nasal symptoms other than anosmia [7], and asthma has not been identified as a mortality risk factor for severe COVID-19 respiratory disease [8]. Instead, chronic non-asthmatic pulmonary diseases are associated with poor COVID-19 outcomes [8].