> They analyzed the human genome and SARS-CoV-2 genome to find out that some genes related to ACE in comparison to genes related to ACE2 are more 'expressed' by

> They analyzed the human genome and SARS-CoV-2 genome to find out that some genes related to ACE in comparison to genes related to ACE2 are more 'expressed' by the Covid-19 virus than normally and they observed known biochemical pathways that are hypothesized to lead to too much bradykinine. FTFY. They didn't measure patients. They modeled genomic interactions to make some predictions about biochemical effects on patients. Then they noted that some of those predicted effects correlate with symptoms of Covid patients. They went further and shotgunned a list of treatments which are known to affect the same biochemical processes. The farther along the path of inference, the weaker the conclusions get, but it sounds like a promising arrow for research to me. > why they couldn't just measure bradykinine levels directly? Is that too hard? Don't need nearly as much permission or human resources to run computer simulations on offline data as you do to take measurements of patients in the hospital.