Additionally, the pathophysiology of COVID-19 is highly heterogeneous, and the way of SARS-CoV-2 modulates the different systems of the host remains unidentified, despite recent discoveries such as viral nucleocapsid (N) protein can bind host mRNA to impair host stress response (Nabeel-Shah et al., 2022); viral infection-induced host hypoxia status can modulate ACE2 expression (Prieto-Fernández et al., 2021); and the overexpression of viral nsp9 can reduce the host’s nucleoporin 62 expression to defective nuclear pore complex formation (Makiyama et al., 2021). The gene discussed is ACE2; the disease is viral infectious disease.