Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of COVID-19, enters cells via the interaction between its spike protein and angiotensin-converting enzyme 2 (ACE-2) and thereby induces systemic inflammation and organ dysfunction by activating the NF-κB-associated inflammasome and producing a downstream cytokine storm [2,3,4]. This evidence concerns the gene ACE2 and COVID-19.