In COVID-19, it has been stated as disproportionately upregulated as a result of ACE2 activity loss upon viral entry or/and direct viral activation of p38 MAPK; the activated p38 MAPK pathway facilitates viral entry via ACE2 endocytosis and predisposes for pathological processes, such as inflammation and thrombosis [237]. The gene discussed is ACE2; the disease is COVID-19.