The severe disease is characterized by an unbalanced host response to SARS-CoV-2, which, following intracellular viral replication, induces a reduction in innate antiviral defenses leading to the exuberant production of pro-inflammatory cytokines/chemokines, with inadequate recruitment of inflammatory populations of monocytes and macrophages with decreased cell surface expression of ACE2, thus losing a lung protective mechanism, leading to increased inflammation, oedema and more severe ARDS, and increased cardiovascular and multi-organ involvement, increasing the risk of thromboembolism. The gene discussed is ACE2; the disease is Thromboembolism.