Summarizing, AKI in patients with COVID-19 has a multifactorial origin, as previously detailed: (a) direct cytopathic action of the virus on kidney tissue through the angiotensin-converting enzyme 2 (ACE-2) receptor to invade host cells; (b) deposition of immune complexes of viral antigens or specific immunological effector mechanisms induced by viruses; (c) indirect effects of cytokines or mediators induced by the virus on kidney tissue; (d) kidney hypoperfusion, vascular coagulation, hypoxia, shock, and rhabdomyolysis; and (e) direct viral aggression and injury of kidney tubules (Figure 2). The gene discussed is ACE2; the disease is COVID-19.