Experimental and epidemiological studies evidenced that SARS-CoV-2 can infect and damage target renal epithelial cells expressing ACE-2 and TMPRSS2, triggering a cytokine storm (sustained especially by IL-6 and interferon) and directly causing AKI by increasing vascular permeability, shock, and multiorgan failure or aggravating/perpetuating a kidney injury already initiated by non-viral processes (37, 38, 42). The gene discussed is TMPRSS2; the disease is acute kidney injury.