SARS-CoV-2 binding to ACE2, and Ang II-induced activation of AT1R, and activation of complement pathways by SARS-CoV-2 may induce assembly of the NLRP3 inflammasome (33–35), which contributes to the onset of cytokine storm, pneumonia, ARDS, thrombosis, DIC, and other types of organ dysfunction (35–37). The gene discussed is NLRP3; the disease is susceptibility to pneumonia measurement.