Virus-occupied ACE2 might weaken their intrinsic function, which could enhance inflammatory response, neutrophils accumulation, and vascular permeability, and ultimately result in influenza-like symptoms, even severe acute respiratory distress syndrome among SARS-CoV-2 infected individuals [47], whereas in the kidneys, elevated immune response made it easier to develop glomerular diseases, such as MN (Figure 1). Here, ACE2 is linked to glomerular disorder.