Importantly, the team also proposed the theory of “malignant circulation” for SARS-CoV-2 invasion of the kidney; that is, in the early stage of SARS-CoV-2 invasion of the kidney, it mainly binds ACE2 (the expression level is higher than that of KIM1 in the physiological state), and after virus-induced acute kidney injury, the expression level of KIM1 is upregulated, thus promoting secondary viral infection mediated by KIM1 and ACE2, aggravating kidney injury and further upregulating KIM1. The gene discussed is ACE2; the disease is acute kidney injury.